The ICD defines stuttering as a "Speech that is characterized by frequent repetitions or prolongations of sounds or syllables or words, or by frequent hesitations or pauses that disrupt the rhythmic flow of speech. It should be classified as a disorder only if its severity is such as to markedly disturb the fluency of speech." (WHO, 2007: F98.5). Since the differences found between stutterers and nonstutterers could't be the direct manifestations of stuttering but the reactions of the subjects to stuttering, we must study the affected subjects before they develop facing reactions: we must study stuttering preschoolers. Stuttering is a typically childhood disease: it begins in 5% of all the children between 16 to 66 months of age (average: 33 months of age); the risk to begin to stutter after the 5th year of age is very low (Yairi & Ambrose, 2005). This is the period of the greatest and fastest development in anatomo-physiological structures and functions, and in linguistic, cognitive and motor abilities as well. Spontaneous recovery occurs in 4 out of 5 children and, most of the times, it takes place within 32 months after the stuttering onset. Although the etiology is still unknown, genetic research established that stuttering is genetically transmitted, but the responsible mechanism at this level is still unknown (Riaz et al., 2005; Suresh et al., 2006). A number of brain structural and functional anomalies have been evidenced in adult stutterers (Brown et al., 2005). Since similar findings have been documented also in children (Chang et al., 2008; Watkins et al., 2008) both developmental stuttering and adult stuttering seem to rely on possibly shared dysfunctional cerebral mechanisms. This don't exclude complete recovery in early childhood due to high neural plasticity (Ludlow et al., 2008). We know that normal children are more disfluent when they produce new syntactic structures (Wijnen, 1990). According to Rispoli et al. (2008), increases in MLU parallel increases in revisions (i.e, "normal" disfluencies), but not in "stallings" (i.e., part-word disfluencies, characteristic of stuttering). According to Howell & Au-Yeung (2002), stallings emerge from a time-lag device children use when they experiment dissynchronies between linguistic planning and motor execution. However, we must be cautious about attributing disfluencies and slowness only to language planning, because increases in language complexity are tied also to increases in speech planning (Smith et al. 2010). Stuttering children are not different from nonstutterers, in the average, as to linguistic structures or psycholinguistic skills, but lower and upper performers are over-represented (Hubbard-Seery et al. 2007) and there are more frequent dissociations in stuttering children than nonstuttering ones among linguistic (higher than normal), phonetic and motor skills (lower than normal, Anderson et al. 2005; Coulter et al. 2009). Good news for phoneticians: although the main predictor of chronicity is biological (to have persistent stutterers among relatives), the second one is phonetic in nature: there are some perceptual and acoustic evidences that very early individuate stuttering children that later will recover from the persistent (the % of "stuttering-like disfluencies" over the total number of disfluencies and the degree of CV coarticulation, Yairi & Ambrose, 2005).
