Congenital and Acquired Amusia as Categories of CAPD (Part 2)

Carrie M. Clancy, B.A., M.M.
Graduate Student, Department of Speech, Language and Hearing Sciences, University of Arizona

 

Part 1 of this article provided a brief overview of congenital and acquired amusia as forms of CAPD. Part 2, presented here, is intended to suggest potential avenues for continued research regarding both congenital and acquired amusias.

 

Congenital Amusia

Subtypes of Congenital Amusia

Use of the plural term “congenital amusias” is an indication of the direction, or multiple directions, future research on the topic might take. “[I]ts use in the plural aims to acknowledge the possibility of various forms of congenital amusia, similar to the various forms that exist for acquired amusia.” “The potential variety of this disorder is further supported by the recent progress of the research domain, now suggesting different subtypes of congenital amusia.” (Tillman et al. 2015)

The majority of research on congenital amusia has focused on the pitch domain. Pitch perception and discrimination difficulties are well-documented in the literature, but recent studies have investigated the specific aspect of pitch memory, theorizing that a deficit in short-term pitch memory might be the basis of impairment for pitch-related congenital amusia. Tillman et al (2015) point out that “memory capacities are required in both pitch discrimination (and) pitch direction tasks” such as the scale, contour, and interval tests on the Montreal Battery for Evaluation of Amusia (MBEA). Studies demonstrating amusics’ short-term pitch memory impairment, both alongside and in the absence of elevated pitch discrimination thresholds, include those by Gosselin et al (2009) and Williamson and Stewart (2010). Additionally, Marin et al (2012) confirmed a similar short-term memory deficit for musical tone and timbre sequences in amusics, and further demonstrated that the deficit was unrelated to specific timbre discrimination ability. Because performance on pitch perception tasks depends on pitch memory, and because conversely, accurate pitch memory depends on accurate pitch perception, further research is needed to more clearly differentiate between perception and memory abilities, and to develop assessments that are sensitive to each.

Ayotte et al (2002) suggested that amusics’ impairments in the time domain, those affecting rhythm and meter, are interrelated “cascade effects of a faulty pitch processing system.” In pyschoacoustic and audiologic terminology, these would be considered temporal processing, and more recent research indicates that such deficits in the time domain might be a discrete problem. Individual cases of amusic impairment solely affecting rhythm and meter have been reported, including those by Phillips-Silver et al (2011) and Bégel et al (2017), among others. Examining deficits in pitch, timbre, rhythm, or meter as independent elements of amusia lends credence to the idea that congenital amusia “is not a unified disorder, but might be a more general terminology,” applicable to a variety of deficits in music perception and production. (Tillman et al, 2015)

 

Congenital Amusia and Speech Processing

Though amusic patients are typically considered to be unimpaired on language tasks as a requisite condition to the amusia diagnosis, recent studies have indicated some correlation between music and speech processing abilities. Thompson et al (2012) has reported emotional processing deficits related to speech prosody and intonation in amusic patients. Jones et al (2009) reported an association in adult subjects between poor performance on the Distorted Tune Test (DTT) and deficits in processing speech sounds. Loui et al (2011) found a “significant positive correlation between pitch perception–production and phonemic awareness” in children, “suggesting that the relationship between musical and linguistic sound processing is intimately linked to awareness at the level of pitch and phonemes” and further hypothesizing that dyslexia (a phonemic awareness disorder) and congenital amusia may have a common or shared neural basis. In their exhaustive literature review regarding dyslexia and auditory temporal processing, Farmer and Klein (1995) found “compelling” evidence for visual and auditory temporal processing deficits as a “significant underlying cause” of developmental dyslexia, and as recently as February 2018, Fostick and Revah suggested auditory temporal processing as part of a “multi-deficit” complex underlying dyslexia. Logic would suggest that auditory temporal processing might play a role in congenital amusia as well. While auditory temporal processing has been examined in relation to acquired amusia, research regarding auditory temporal processing in congenital amusia is still relatively sparse. (See Albouy et al, 2016.)

 

Anatomic Correlates in Congenital Amusia

As stated in Part 1, brain-imaging and electrophysiologic studies have emerged alongside behavioral depictions of congenital amusia. Current research strongly suggests abnormalities in white and gray matter concentrations in amusic brains, which are somewhat analogous to structural abnormalities in adult brains with speech and language disorders. More specifically, Loui et al (2009) found evidence of reduced arcuate fasciculus connectivity in “tone deaf” subjects, as well as suggesting a correlation between arcuate fasciculus branch volume and pitch discrimination ability. According to Tillman (2015), “[These] observed structural differences suggest cortical malformations of a right frontotemporal pathway in the amusic brain, resulting in a pitch-processing impairment.”

Tillman continues,”This hypothesis is consistent with patient data on acquired amusia and with neuroimaging data of the normal, non-amusic brain showing that the right superior temporal cortex is involved in perceptual analyses of melodies and that pitch processing recruits neural networks, including the right frontal cortex.” Peretz et al (2007) have previously suggested that these abnormalities in congenital amusia may have a genetic basis, which should also be further explored.

 

Congenital Amusia and Implications for Rehabilitation

EEG recordings and auditory evoked potentials suggest that congenital amusics have “normal preattentive pitch change detection” but fail to explicitly report pitch incongruities. “These studies suggest that the amusic brain presents abnormalities in the processing of musical material both in the auditory cortices and in the inferior frontal cortices, associated with decreased functional connectivity between the structures.” The distinction between patients’ explicit deficits in awareness and identification of musical elements and their apparently intact implicit perceptual abilities becomes important in the development of rehabilitation strategies. The”spared implicit processing resources” of congenitally amusic patients might be employed therapeutically to reduce or remediate explicit deficits. (Tillman et al, 2015).

It should be noted that, with few exceptions, the study of congenital amusia has focused on adult subjects, though the condition is believed to be present from birth. This is largely a practical consequence of a child’s inability to self-identify as amusic, even in the colloquial sense of being “tone deaf” or “having two left feet.” However, Tillman (2015) points out that developing a full understanding of congenital amusia “is not restricted to the static situation in adulthood (as in most studies up to now), but requires study of its development in children, or even infancy (as started recently), and the development of potential perspectives for rehabilitation.”

 

Acquired Amusia

“Acquired amusia provides a unique opportunity to investigate the fundamental neural architectures of musical processing due to the transition from a functioning to defective music processing system.” (Sihvonen et al 2017)

Even more so than with congenital amusia, acquired amusia has offered opportunities for using functional brain imaging to conduct lesion-led studies and to map the neural networks involved in both normal and impaired music processing. Going a step further, Clark et al (2015) point out that “functional neuroimaging (also) potentially allows an unprecedentedly direct comparison of these substrates with the neural substrates for processing speech and language,” (as well as certain auditory functions).

Recent research is also finding that large-scale, convergent brain networks, such as those involved in music, auditory, and language processing, are particularly vulnerable not only to damage from brain injury or lesion, but also to neurodegenerative conditions such as Alzheimer’s disease. (Zhou et al, 2010; Warren et al, 2013) Further study is needed to identify the music processing networks affected by particular neurodegenerative conditions and to differentiate these from amusias caused by focal brain damage or congenital pathology.

Increasingly accurate neural network mapping, and matching these of neural maps to music cognition and behavior, have led to ongoing revisions in the way we structure our thinking about music processing. As noted above, amusias have most recently been classified by the affected perceptual or cognitive domain (i.e., pitch, rhythm, or timbre). But Clark et al (2015) have proposed a different “framework for understanding amusias essentially as disorders of information processing, informed by contemporary cognitive neuroscience,” and analogous to similar frameworks in visual and linguistic neuroscience.

As Clark et al (2015) note, current assessment instruments for amusia are difficult to use in patients with limited musical training and are “vulnerable to potentially confounding effects, such as reliance on working memory or verbal labeling capacities.” Additionally, patients are more likely to complain of amusic symptoms if they have both intact language skills and prior musical experience. To this end, the authors suggest formulating a test battery for amusias that includes assessment of more nuanced aspects of music cognition, including musical instrument recognition, melody recognition, simultaneous voice/instrument tracking, and altered emotional response. Development of standardized test procedures for amusias will facilitate comprehensive screening for amusic deficits and will also allow for refinements in diagnosis and prevalence reporting.

 

References

Albouy, P., Cousineau, M., Caclin, A., Tillmann, B., and Peretz, I. (2016). Impaired encoding of rapid pitch information underlies perception and memory deficits in congenital amusia. Scientific Reports 6, 18861. http://doi.org/10.1038/srep18861

Ayotte, J., Peretz, I., Hyde, K. (2002). Congenital amusia: A group study of adults afflicted with a music‐specific disorder. Brain, 125(2), 238–251. https://doi.org/10.1093/brain/awf028

Bégel, V., Benoit, C., Correa, A., Cutanda, D., Kotz, S.A., Dalla Bella, S. (2017). “Lost in time” but still moving to the beat. Neuropsychologia, 94, 129-138. http://dx.doi.org/10.1016/j.neuropsychologia.2016.11.022

Clark, C. N., Golden, H. L., & Warren, J. D. (2015). Acquired amusia. In G. G. Celesia & G. Hickok (Eds.), The human auditory system: Fundamental organization and clinical disorder /series editors, Michael J. Aminoff, Francois Boller, and Dick F. Swaab (1st ed., Vol. 129, Ser. 3, pp. 607-631). Edinburgh etc.: Elsevier.

Farmer, M.E., and Klein, R.M. (1995). The evidence for a temporal processing deficit linked to dyslexia: A review. Psychonomic Bulletin and Review, 2(4), 460-493. https://doi.org/10.3758/BF03210983

Fostick, L. and Revah, H. (2018). Dyslexia as a multi-deficit disorder: Working memory and auditory temporal processing. Acta Psychologia, 183, 19-28. https://doi.org/10.1016/j.actpsy.2017.12.010

Gosselin, N., Jolicoeur, P., and Peretz, I. (2009). Impaired memory for pitch in congenital amusia. Annals of The New York Academy of Sciences, 1169(1), 270-272. https://doi.org/10.1111/j.1749-6632.2009.04762.x

Jones, J.L., Lucker, J., Zalewski, C., Brewer, C., and Drayna, D. (2009). Phonological processing in adults with deficits in musical pitch recognition. Journal of Communication Disorders, 42, 369-382. https://doi.org/10.1016/j.jcomdis.2009.01.001

Loui, P., Alsop, D., and Schlaug, G. (2009). Tone Deafness: A New Disconnection Syndrome? The Journal of Neuroscience, 29(33):10215–10220. https://doi.org/10.1523/JNEUROSCI.1701-09.2009

Loui, P., Kroog, K., Zuk, J., Winner, E., and Schlaug, G. (2011). Relating pitch awareness to phonemic awareness in children: Implications for tone-deafness and dyslexia. Frontiers in Psychology, 2, 111. https://doi.org/10.3389/fpsyg.2011.00111

Marin, M.M., Gingras, B., and Stewart, L. (2012). Perception of musical timbre in congenital amusia: Categorization, discrimination and short-term memory. Neuropsychologia, 50, 367-378. https://doi.org/10.1016/j.neuropsychologia.2011.12.006

Peretz, I., Cummings, S., and Dubé, M.P. (2007). The genetics of congenital amusia (tone deafness): A family-aggregation study. American Journal of Human Genetics, 81(3), 582-588. https://doi.org/10.1086/521337

Phillips-Silver, J., Toiviainen, P., Gosselin, N., Piché, O., Nozaradan, S., Palmer, C., and Peretz, I. (2011). Born to dance but deaf: a new form of congenital amusia. Neuropsychologia, 49, 961-969. https://doi.org/10.1016/j.neuropsychologia.2011.02.002

Sihvonen, A.J., Ripollés, P., Särkämö, T., Leo, V., Rodrígues-Fornells, A., Saunavaara, J., Parkkola, R., and Soinila, S. (2017). Tracting the neural basis of music: Deficient structural connectivity underlying acquired amusia. Cortex, 97, 255-273. https://doi.org/10.1016/j.cortex.2017.09.028

Thompson, W.F., Marin, M.M., and Stewart, L. (2012). Reduced sensitivity to emotional prosody in congenital amusia rekindles the musical protolanguage hypothesis. Proceedings of the National Academy of Sciences, 109(46), 19027-19032. https://doi.org/10.1073/pnas.1210344109

Tillmann, B., Albouy, P., and Caclin, A. (2015). Congenital amusias. In G. G. Celesia & G. Hickok (Eds.), The human auditory system: Fundamental organization and clinical disorder /series editors, Michael J. Aminoff, Francois Boller, and Dick F. Swaab (1st ed., Vol. 129, Ser. 3, pp. 589-605). Edinburgh etc.: Elsevier.

Warren, J.D., Roher, J.D., Schott, J.M., Fox, N.C., Hardy, J., and Rosser, M.N. (2013). Molecular nexopathies: a new paradigm of neurodegenerative research. Trends in Neurosciences, 36, 561-569. https://doi.org/10.1016/j.tins.2013.06.007

Williamson, V.J., and Stewart, L. (2010). Memory for pitch in congenital amusia: beyond a fine-grained pitch discrimination problem. Memory, 18(6), 657-669.  https://doi.org/10.1080/09658211.2010.501339

Zhou, J., Greicius, M.D., Gennatas, E.D., Growdon, M.E., Jang, J.Y., Rabinovici, G.D., Kramer, J.H., Weiner, M., Miller, B.L., Seeley, W.W. (2010). Divergent network connectivity changes in behavioural variant frontotemporal dementia and Alzheimer’s disease. Brain, 133, 1352-1367.

 

Carrie Clancy is a graduate student in Audiology at the University of Arizona. She has received Bachelor of Arts degrees in Music and Speech-Language Pathology/Audiology and a Master of Music degree from the University of Nebraska. She will begin the Au.D. program at the University of Arizona in Fall 2018.

About Pathways

Pathways is both a column that covers topics related to CAPD and Neuroaudiology and a society for people interested in central auditory disorders that regularly meets to discuss these issues.

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