Although both target articles develop compelling theories on the evolutionary origins of music, the current commentary will focus on the neurobiological model underlying the music and social bonding (MSB) hypothesis. In their model, the authors propose key neural systems underlying the social bonding function of music. Accordingly, they predict that individuals with disruptions to these neural systems may show altered responses to music. One such prediction is that “special populations with high sociability may respond well to musical features especially when coupled with social stimuli” (sect. 5.4, para. 2). Although it is not exactly clear what “respond well” means in this case (let's assume this means that individuals with heightened sociability will also show heightened social and/or emotional responsiveness to music), one could also consider the converse prediction, that individuals with abnormally low social functioning may not respond emotionally to music.

When thinking of populations with disrupted social functioning, one can look toward the neuropsychological literature: A rich history of literature demonstrates that individuals with damage to the ventromedial prefrontal cortex (vmPFC) show substantial changes in their social and affective behaviors (for review, see Schneider & Koenigs, Reference Schneider and Koenigs2017). The vmPFC is highlighted by Savage and colleagues as a critical component of the neuroanatomical model underlying the MSB hypothesis (see Fig. 3). Because the authors claim that this system is “involved causally in the link between music and social bonding” (sect. 4.2, para. 2), a useful approach might be to consider whether the behavior of individuals with damage to the vmPFC aligns with its proposed role underlying the social function of music.

To address this point, the current commentary will focus on research investigating the behavior of individuals with lesions to the vmPFC and consider these findings with regard to the predictions put forth by the MSB hypothesis. To start, substantial prior research has indicated that individuals with damage to the vmPFC have deficits in various socioemotional domains, including emotion and reward, social behavior, and value-based decision-making (Abel et al., Reference Abel, Manzel, Bruss, Belfi, Howard and Tranel2016; Jenkins et al., Reference Jenkins, Andrewes, Nicholas, Drummond, Moffat, Phal and Kessels2014). For example, individuals with vmPFC damage show both functional and structural disruptions to the reward network, including decreased nucleus accumbens volumes and reduced activity in the ventral striatum during the anticipation of reward (Pujara, Philippi, Motzkin, Baskaya, & Koenigs, Reference Pujara, Philippi, Motzkin, Baskaya and Koenigs2016). In addition, individuals with vmPFC damage display deficits in social cognition and behavior, including theory of mind (Leopold et al., Reference Leopold, Krueger, Dal monte, Pardini, Pulaski, Solomon and Grafman2012), moral decision-making (Koenigs et al., Reference Koenigs, Young, Adolphs, Tranel, Cushman, Hauser and Damasio2007), and empathy (Beadle, Paradiso, & Tranel, Reference Beadle, Paradiso and Tranel2018).

The authors of the MSB hypothesis imply that individuals with disrupted social functioning, such as persons with vmPFC damage, should also display considerable deficits in the socioemotional aspects of music. Some evidence does point toward impaired music processing in individuals with vmPFC damage. For example, persons with vmPFC damage show reduced skin conductance responses in response to music, indicating a lack of physiological arousal (Johnsen, Tranel, Lutgendorf, & Adolphs, Reference Johnsen, Tranel, Lutgendorf and Adolphs2009). Individuals with vmPFC damage also produce music-evoked autobiographical memories that are less episodically rich, as compared to memories evoked by visual cues (Belfi, Karlan, & Tranel, Reference Belfi, Karlan and Tranel2018). Other research in patients with behavioral variant frontotemporal dementia (bvFTD) suggests that the vmPFC plays a critical role in “mentalizing” in music. That is, patients with bvFTD have difficulties attributing complex mental states to music (e.g., identifying whether music sounds “dreamy,” “dreading,” or “adventurous”). Interestingly, this deficit in musical emotion attribution was correlated with deficits in social inference and empathy more broadly, and was associated with gray matter loss in the vmPFC (Downey et al., Reference Downey, Blezat, Nicholas, Omar, Golden, Mahoney and Warren2013). Taken together, this research suggests that individuals with damage to the vmPFC have both deficits in social cognition and affect more broadly, as well as in their emotional responses to music.

Although the aforementioned research suggests that the vmPFC plays a critical role underlying the social and emotional aspects of musicality, it does not seem that vmPFC damage leads to a complete disregard for music. That is, individuals with vmPFC damage do not exhibit higher levels of musical anhedonia (a selective lack in pleasure from music). No published cases of acquired musical anhedonia include damage to the vmPFC (Griffiths, Warren, Dean, & Howard, Reference Griffiths, Warren, Dean and Howard2004; Hirel et al., Reference Hirel, Leveque, Deiana, Richard, Cho, Mechtouff and Nighoghossian2014; Mazzoni et al., Reference Mazzoni, Moretti, Pardossi, Vista, Muratorio and Puglioli1993; Satoh, Nakase, Nagata, & Tomimoto, Reference Satoh, Nakase, Nagata and Tomimoto2011; Satoh et al., Reference Satoh, Kato, Tabei, Nakano, Abe, Fujita and Kondo2016) and a large-scale lesion study did not identify any persons with vmPFC damage as musically anhedonic (Belfi, Evans, Heskje, Bruss, & Tranel, Reference Belfi, Evans, Heskje, Bruss and Tranel2017). This may be explained by the fact that acquired musical anhedonia is typically characterized by self-reported changes in emotional responses to music. That is, it may be the case that individuals with vmPFC damage do not self-report changes in musical reward, although they might experience reduced musical reward. This coincides with evidence indicating that individuals with vmPFC damage show reduced physiological responsiveness, but not reductions in subjective feelings when listening to music (Johnsen et al., Reference Johnsen, Tranel, Lutgendorf and Adolphs2009).

To conclude, the authors of the MSB hypothesis highlight the role of the reward system, including the vmPFC, as a critical network supporting the coevolved processes of social bonding and music. This model subsequently predicts that damage to structures in this network would disrupt the social bonding effects of music. Although not testing the social bonding effects of music directly, some research indicates that damage to the vmPFC is associated with deficits in socioemotional aspects of music, including physiological responsiveness, music-evoked autobiographical memories, and attributing mental states to music. When taken together, these results provide tentative support for the role of the vmPFC in the socioemotional components of musicality. Although this seems promising for the neurobiological model underlying the MSB hypothesis, there is one final but important point to note – the fact that two cognitive processes are disrupted from damage to the same region (i.e., vmPFC damage is associated with deficits in both social behavior and emotional responses to music) does not necessarily speak directly to the relationship between those processes. Therefore, although it should be interpreted cautiously, this research provides initial evidence for similar neural systems underlying both social behavior and emotional responses to music.