Voiced cries are described as cries where the fundamental frequency is well evident in the spectrogram, while voiceless and partially voiced cries partially or totally lack a well defined contour (Lieberman 1985: In Infant crying: Theoretical and research perspectives. (B. M. Lester & C. F. Z. Boukydis, eds.) Plenum Press; New York pp. 29-58). Some authors suggest that a greater percentage of the latter is pathognomonic of CNS damage, as happens in kernicterus due to hyperbilirubinemia (Koivisto 1987: Acta Paediatrica Scandinavia Suppl. 335, 1-73). In a study of the ontogeny of premature infant cries carried in our laboratory, we found a greater amount of voiceless and partially voiced cries in premature infants aged 34 and 40 weeks than in normal control. However, normal infants show a considerable amount of voiceless and partially voiced cries (Lenti Boero et al. 1998, Perceptual & Motor Skills 86, 1123-1140), while infants affected by severe pathologies such as congenital hypothyroidism (Lenti Boero et al. 2000: J. Child Neurology 15, 603-608) and CNS lesions induced by neonatal asphyxia, emit a lesser amount of voiceless and partially voiced cries than normal controls. In this presentation we examine this issue, both from a physioacoustic and an evolutionary perspective and suggest that disphonation might be due to different causes and that in normal infants it might have had an important evolutionary role in calling the attention of a distant care-giver.