Any account of “what is special about the human brain” (Passingham 2008) must specify the neural basis of our unique ability to produce speech and delineate how these remarkable motor capabilities could have emerged in our hominin ancestors. Clinical data suggest that the basal ganglia provide a platform for the integration of primate-general mechanisms of acoustic communication with the faculty of articulate speech in humans. Furthermore, neurobiological and paleoanthropological data point at a two-stage model of the phylogenetic evolution of this crucial prerequisite of spoken language: (i) monosynaptic refinement of the projections of motor cortex to the brainstem nuclei that steer laryngeal muscles, presumably, as part of a “phylogenetic trend” associated with increasing brain size during hominin evolution; (ii) subsequent vocal-laryngeal elaboration of cortico-basal ganglia circuitries, driven by human-specific FOXP2 mutations.;>This concept implies vocal continuity of spoken language evolution at the motor level, elucidating the deep entrenchment of articulate speech into a “nonverbal matrix” (Ingold 1994), which is not accounted for by gestural-origin theories. Moreover, it provides a solution to the question for the adaptive value of the “first word” (Bickerton 2009) since even the earliest and most simple verbal utterances must have increased the versatility of vocal displays afforded by the preceding elaboration of monosynaptic corticobulbar tracts, giving rise to enhanced social cooperation and prestige. At the ontogenetic level, the proposed model assumes age-dependent interactions between the basal ganglia and their cortical targets, similar to vocal learning in some songbirds. In this view, the emergence of articulate speech builds on the “renaissance” of an ancient organizational principle and, hence, may represent an example of “evolutionary tinkering” (Jacob 1977).

Two substantive issues are relevant to discussions of the evolution of acoustic communication and merit further consideration here. The first is the importance of communicative ontogeny and the impact of the proximal social environment on the early development of communication and language. The second is the emerging evidence for a number of non-linguistic roles of FOXP2 and its orthologs.

Unlike nonhuman primates, thousands of bird species have articulatory capabilities that equal or surpass those of humans, and they develop their vocalizations through vocal imitation in a way that is very similar to how human infants learn to speak. An understanding of how speech mechanisms have evolved is therefore unlikely to yield key insights into how the human brain is special.

Language production is a multilevel phenomenon, and human capacities to communicate vocally progress from early forms, based on projections of motor cortex to brainstem nuclei, to complex elaborations, mediated by high-order cognition and fostered by socially mediated feedback.

Ackermann et al. briefly point out the potential significance of coordinated vocal behavior in the dual pathway model of acoustic communication. Rhythmically entrained and articulated pre-linguistic vocal activity in early hominins might have set the evolutionary stage for later refinements that manifest in modern humans as language-based conversational turn-taking, joint music-making, and other behaviors associated with prosociality.

FOXP2 expression in the evolution of language derives from its role in allowing vocal articulation that is sensitive to its consequences. The discrete verbal discourse it allows must have evolved recently relative to affective features of vocal behavior such as tone of voice. Because all organ systems must have evolved in the service of behavior, attention is given to ways in which environments may have driven brain organization.

Contradicting new dual-pathway models of language evolution, cortico-striatal-thalamic circuitry disambiguate uncertainties in affective prosody and propositional linguistic content of language production and comprehension, predictably setting limits on useful complexity of articulate phonic and/or signed speech. Such limits likely evolved to ensure public information is discriminated by intended communicants and safeguarded against the ecological pressures of social eavesdropping within and across phylogenetic boundaries.

We present two arguments why physical adaptations for vocalization may be as important as neural adaptations. First, fine control over vocalization is not easy for physical reasons, and modern humans may be exceptional. Second, we present an example of a gorilla that shows rudimentary voluntary control over vocalization, indicating that some neural control is already shared with great apes.

Recent evidence from very young human infants' responses to human and nonhuman primate vocalizations offers new insights – and brings new questions – to the forefront for those who seek to integrate primate-general and human-specific mechanisms of acoustic communication with theories of language acquisition.

Neuroimaging studies have verified the important integrative role of the basal ganglia during affective vocalizations. They, however, also point to additional regions supporting vocal monitoring, auditory–motor feedback processing, and online adjustments of vocal motor responses. For the case of affective vocalizations, we suggest partly extending the model to fully consider the link between primate-general and human-specific neural components.

We support Ackermann et al.'s proposal that the cortico-basal ganglia circuits may play essential roles in the evolution of spoken language. Here we discuss further evidence indicating that the cortico-basal ganglia circuits may contribute to various aspects of spoken language including planning, learning, and controlling of speech in adulthood.

Ackermann et al.'s phylogenetic account of speech argues that the basal ganglia imbue speech with emotive content. However, a body of work on auditory/emotive processing is inconsistent with attributing this function exclusively to these structures. The account further overlooks the possibility that the emotion-integration function may be at least in part mediated by the cortico-ponto-cerebellar system.

The gradual audiomotor evolution hypothesis is proposed as an alternative interpretation to the auditory timing mechanisms discussed in Ackermann et al.'s article. This hypothesis accommodates the fact that the performance of nonhuman primates is comparable to humans in single-interval tasks (such as interval reproduction, categorization, and interception), but shows differences in multiple-interval tasks (such as entrainment, synchronization, and continuation).

Ackermann et al. treat both genetic and paleoanthropological data too superficially to support their conclusions. The case of FOXP2 and Neanderthals is a prime example, which I will comment on in some detail; the issues are much more complex than they appear in Ackermann et al.

Ackermann et al. provide an informative neurological road-map to primate call communication. However, the proposed model for speech evolution inadequately integrates comparative primate evidence. Critically, great ape voiceless calls are explicitly rendered unimportant, leaving the proposed model deprived of behavioral feedstock and proximate selective drivers capable of triggering the neurological transformations described by the authors in the primate brain.

Building a theory on extant species, as Ackermann et al. do, is a useful contribution to the field of language evolution. Here, I add another living model that might be of interest: human language ontogeny in the first year of life. A better knowledge of this phase might help in understanding two more topics among the “several building blocks of a comprehensive theory of the evolution of spoken language” indicated in their conclusion by Ackermann et al., that is, the foundation of the co-evolution of linguistic motor skills with the auditory skills underlying speech perception, and the possible phylogenetic interactions of protospeech production with referential capabilities.

Ackermann et al. disregard attested knowledge concerning aphasia, Parkinson disease, cortical-to-striatal circuits, basal ganglia, laryngeal phonation, and other matters. Their dual-pathway model cannot account for “what is special about the human brain.” Their human cortical-to-laryngeal neural circuit does not exist. Basal ganglia operations, enhanced by mutations on FOXP2, confer human motor-control, linguistic, and cognitive capabilities.

Research on acoustic communication and its underlying neurobiological substrates has led to new insights about the functioning of central pattern generators (CPGs). CPG-related atypicalities may point to brainstem irregularities rather than cortical malfunctions for early vocalizations/babbling. The “vocal pattern generator,” together with other CPGs, seems to have great potential in disentangling neurodevelopmental disorders and potentially predict neurological development.

In self-adapting dynamical systems, a significant improvement in the signaling flow among agents constitutes one of the most powerful triggering events for the emergence of new complex behaviors. Ackermann and colleagues' comprehensive phylogenetic analysis of the brain structures involved in acoustic communication provides further evidence of the essential role which speech, as a breakthrough signaling resource, has played in the evolutionary development of human cognition viewed from the standpoint of complex adaptive system analysis.

We argue that a comprehensive model of human vocal behaviour must address both voluntary and involuntary aspects of articulate speech and non-verbal vocalizations. Within this, plasticity of vocal output should be acknowledged and explained as part of the mature speech production system.