Focal brain lesions causing acquired amusia map to a common brain network

Music is a universal human attribute. The study of amusia, a neurologic music processing deficit, has increasingly elaborated our view on the neural organization of the musical brain. However, lesions causing amusia occur in multiple brain locations and often also cause aphasia, leaving the distinct neural circuits for amusia unclear. Here, we utilized lesion network mapping to identify these circuits. A systematic literature search was carried out to identify all published case reports of lesion-induced amusia. The reproducibility and specificity of the identified amusia network were then tested in an independent prospective cohort of 97 stroke patients (46 female and 51 male) with repeated structural brain imaging, specifically assessed for both music perception and language abilities. Lesion locations in the case reports were heterogenous, but connected to common brain regions, including bilateral temporoparietal and insular cortices, precentral gyrus, and cingulum. In the prospective cohort, lesions causing amusia mapped to a common brain network, centering on the right superior temporal cortex and clearly distinct from the network causally associated with aphasia. Lesion-induced longitudinal structural effects in the amusia circuit were confirmed as reduction of both grey and white matter volume, which correlated with the severity of amusia. We demonstrate that despite the heterogeneity of lesion locations disrupting music processing, there is a common brain network, that is distinct from the language network. These results provide evidence for the distinct neural substrate of music processing, differentiating music-related functions from language, providing a testable target for non-invasive brain stimulation to treat amusia. Significance Statement Perspectives on the neural organization of language and music have been elaborated by studying the respective brain lesion induced deficits, aphasia and amusia, but without leading to an agreement regarding their shared and distinct neural circuitries. This study demonstrates that lesions disrupting music processing map to a common brain network, which is distinct from speech processing networks in the brain. Importantly, our data confirms, the lesion-induced longitudinal structural effects in the central nodes of the amusia network, resulting in both grey and white matter atrophy. The results lend insight into the neural substrate of music processing, add neural evidence for the differentiability of music-related functions from language, and provide first testable targets for non-invasive brain stimulation to treat amusia.