Ashley DeMato and Gabriella Wilkinson

Thompson et al. (2012) examined reduced sensitivity to emotional prosody in individuals with Congenital Amusia. Congenital Amusia is a neurodevelopmental disorder characterized by deficits in processing acoustic and structural attributes of music (Thompson et al. 2012). The goal of this study was to examine if individuals with this disorder have difficulties with interpreting music and if their ability to perceive emotional prosody of music is impaired as well. According to Thompson, “several evolutionary theories assume that music and language have a common origin as an emotional protolanguage that remains evident in overlapping functions and shared neural circuitry” (Thompson et al. 2012). Researchers then began to hypothesize that sensitivity to emotion in speech prosody derives from the capacity to process music. So if an individual’s capacity to process and interpret music is impaired then sensitivity to emotional speech prosody should be impaired as well. The Musical Protolanguage Hypothesis resurfaced due to the original idea that sensitivity to music – a channel specialized for emotional communication – should be correlated with sensitivity to emotion conveyed by speech (Thompson et al. 2012).

Twelve individuals with Congenital Amusia and twelve matched-control participants were used within this study. Thompson et al. (2012) used the Montreal Battery of Evaluation of Amusia (MBEA) to assess each individual’s ability to perceive emotional expressions within 96 spoken phrases. Each phrase was semantically neutral and included prosodic cues (tone of voice) communicated through 6 different emotional states: happy, tender, afraid, irritated, sad, and no emotion (Thompson et al. 2012). Behavioral manifestations were also recorded for both groups of participants.

Findings show that, “Congenital Amusia individuals performed significantly worse than the control participants at decoding emotional prosody, with decoding rates of emotions up to 20% lower than matched controls” (Thompson et al. 2012). In other words, amusic individuals were less accurate when trying to depict what emotion was being expressed in the phrases. These individuals also reported having difficulty with understanding emotional prosody in daily life, suggesting some awareness of the deficit (Thompson et al. 2010). This specific finding directly relates to the individual’s behavioral manifestations recorded throughout the study. Amusic individuals report fewer changes in emotional state while listening to music and do not incorporate music into their daily life to the extent reported by most people (Thompson et al. 2012). Overall these findings support speculations that music and language share mechanisms that trigger emotional responses to acoustic attributes, as predicted by theories that propose a common evolutionary link between these domains. This begins to explain the complexity of evidence suggesting Congenital Amusia no longer only applies when interpreting music. Evidence shows that individuals with congenital amusic also struggle with basic social interaction – such as when these individuals try to accurately perceive the connotation of emotional speech.

For this specific study, researchers focused more on the behavioral manifestations of amusic individuals and how they respond to speech. In previous studies, researchers focused more heavily on the structural brain differences found in individuals suffering from Congenital Amusia. When researchers started to look at the brains of amusic individuals they found subtle structural differences in these individuals compared to the matched-controls. There were subtle differences in both the inferior frontal cortex and superior temporal areas – variously in the left or right hemispheres (Thompson et al. 2012). Further research has found relations between the neuroscience of amusic brains and impaired pitch perception and memory. Subjects in this study were asked to perform melodic tasks where they had to indicate whether six tones were the same or different. The major findings by Albouy and his colleagues was that pitch processing and short-term memory deficits can be traced down to amusics’ early brain responses. Temporal and frontal generators were abnormally recruited in the amusic brain. Results revealed decreased intrinsic connectivity in both auditory cortices, increased lateral connectivity between auditory cortices as well as a decreased right fronto-temporal backward connectivity. Abnormal functioning of this fronto-temporal network was also prevalent. Morphological brain anomalies were found in terms of white and grey matter, as well, which plays a major role in the connection and communication of the brain processes. The relation between functional and structural brain differences supports the hypothesis of abnormalities in the cerebral pathways of the amusic brain, specifically of the front-temporal pathway. This study provides first evidence of affected functioning and structure of the auditory cortices during pitch perception and memory in congenital amusia.

Congenital amusia is a neurodevelopmental disorder of musical perception as well as production. Through Thompson et al. (2012) and Albouy et al. (2013), further research should be done to develop more extensive intervention strategies and therapeutic forms for those with congenital amusia. Therapists can take the information provided about the altered states of amusic brains and help individuals work on their inability to decipher emotional connotations of speech.

 

References

 

Albouy, P., Mattout, J., Bouet, R., Maby, E., Sanchez, G., Aguera, P.E., Daligault, S., Delpuech, C., Bertrand, O., Caclin, A., Tillmann, B. (2013). Impaired Pitch Perception and Memory in Congenital Amusia: The Deficit Starts in the Auditory Cortex. Oxford University Press; p 1639-1661.

Thompson, W. F., Marin, M. M., & Stewart, L. (2012). Reduced sensitivity to emotional prosody in congenital amusia rekindles the musical protolanguage hypothesis. PNAS,
109,
19027-19032.

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Psychology of Language Copyright © 2017 by Maureen Gillespie, PhD is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted.

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