This study investigates the use of the basicrania of fossil hominids as a guide to reconstructing their possible upper respiratory systems. As described previously (Laitman and Crelin, '76; Laitman et al., '781, the exocranial orientation of the basicrania of extant primates is related to the position of upper respiratory structures such as the larynx and pharynx. These relationships in living primates suggest that the basicraniurn of fossil hominids may provide an indicator of what their upper respiratory systems were like.Originals and casts of 14 fossil hominids were examined. The marked similarities in overall basicranial form between Sterkfontein 5 and extant pongids indicate that Sterkfontein had an upper respiratory system similar to that of extant great apes. The Classic European Neandertals show a range of basicranial, and thus potential upper respiratory, structure comparable to extant human children between 2 and 11 years of age. Cro-Magnon, Steinheim, Pfedmosti, Broken Hill, and the more recent North African hominids, exhibit basicrania much more similar to those of adult or sub-adult modern humans. Their upper respiratory systems probably did not differ considerably from that of present day adult humans. Our craniometric analysis has shown that it is statistically improbable for the basicrania, and by extrapolation, upper respiratory systems of certain Neandertals t o fall within the range of modern adult or sub-adult humans. There thus appear to be at least two different pathways taken in the evolution of man's upper respiratory system after a common pongid-like stage exhibited by the australopithecines. One line appears to have terminated with the Classic Neandertals. The other line, encompassing those hominids with basicrania and upper respiratory structures of more modern appearance, may have given rise t o modern man.

This study investigated the relationship between alterations in a basicranial line and changes in the upper respiratory system of selected nonhuman primates and of man. This was done through multivariate analysis of craniometric measurements which describe midline exocranial flexion, and compares the analytical results with previous postmortem findings on upper respiratory structure and function.Craniometric analysis has shown that the skulls of the non-human primate species studied and those of newborn human infants are relatively non-flexed exocranially between the posterior border of the hard palate and foramen magnum. This finding corresponds to the relatively high position of their upper respiratory structures. In this group the tongue lies entirely within the oral cavity, and the epiglottis is found intranarial.After approximately the second year, humans exhibit marked exocranial flexion between the hard palate and foramen magnum. These basicranial changes coincide with concomitant changes occurring in the positional relationships of the upper respiratory system. After the second year the tongue and larynx have descended considerably into the neck, greatly altering their functional relationships.There thus appears to be a relationship between the exocranial orientation of the basicranium and the positioning of upper respiratory structures. There also appears to be a direct structural, and possible functional, relationship between (1) the position of the larynx, (2) the orientation of the pharyngeal constrictor muscles, and (3) the orientation of the basiocciput.

Our analyses of extant primates have shown that a relationship exists between the degree of flexion of the basicranium and the location of upper respiratory structures such as the larynx and pharynx (Laitman et al., 1978). Based upon these relationships, we have previously used the basicrania of late Pleistocene hominids as a guide to the reconstruction of their upper respiratory anatomy (Laitman et al., 1979). This study continues our approach by examining the basicrania of Plio-Pleistocene hominids and reconstructing their upper respiratory systems. Nine Plio-Pleistocene hominids had basicrania complete enough to be used in this study. These included the originals of Sts 5, MLD 37/38, SK 47, SK 48, SK 83, Taung, KNM-ER 406, OH 24, and a cast of OH 5. Craniometric analysis of the basicrania of these specimens showed that they had marked similarities to those of extant pongids. These basicranial similarities between Plio-Pleistocene hominids and extant apes suggest that the upper respiratory systems of these groups were also alike in appearance. As with living nonhuman primates, the early hominids probably exhibited a larynx and pharynx positioned high in the neck. This high position would have permitted an intranarial epiglottis to be present during both normal respiration and the ingestion of a liquid bolus of food. The high position of the larynx would have also greatly restricted the supralaryngeal portion of the pharynx available to modify laryngeal sounds. It is thus possible that the Plio-Pleistocene hominids exhibited modes of breathing, swallowing and vocalizing similar to those of living apes.

Handedness and its possible inheritance have been studied in a colony of 69 Macaca radiata by observation of hand usage during daily feeding and foraging activities. Each animal was observed for the number of right- and left-handed actions made during two tasks:feeding and searching. Individual animals fell into one of three classes: significantly right-handed, significantly left-handed, and no significant preference. For analysis, handedness was considered as both a directional phenomenon (percentage right-handed usage) and a degree phenomenon (absolute deviation from 50:50 hand usage). Feeding and searching were significantly correlated for both direction and degree. Therefore, laterality for handedness does exist in this primate species. A developmental aspect to laterality was suggested by the positive correlation of degree with age. No mother-offspring correlations were found for either direction or degree and half-sibships were not more similar for either. Thus, there is no evidence for a genetic component to either direction or degree of handedness.

Stuttering is not usually considered genetic, although it has long been known to be familial. Data collected on 2035 relatives of397 unrelated adult stutterers confirm and quantify the strong familial concentration. Our analytic approach to these family data, one that does not require specification of a genetic hypothesis, shows that stuttering among relatives occurs in a pattern indicating vertical transmission ofa susceptibility to stuttering with sex-modified expression. Although simple Mendelian hypotheses are not sufficient to explain the observed pattern of stuttering in families, more complex genetic models can explain the pattern. In the past, such evidence has been considered sufficient, because it does not preclude the possibility of cultural transmission. However, certain cultural transmission hypotheses previously proposed for stuttering are excluded by these data. The findings in this study support a growing opinion among speech pathologists that most stuttering is a genetically inherited neurologic disorder.Stuttering is a readily identifiable disorder of speech characterized by frequent interruptions or blocks in the smooth transition from the production of one sound to the production of the subsequent sound. The primary defect in stuttering, the block, is manifest as a repetition or prolongation of a sound, or as a silent gap in speech (1, 2). A layman's recognition of these symptoms and judgement of the presence of stuttering correspond closely to a speech pathologist's. The block is believed to reflect a basic organic problem (1, 2). Aberrant laryngeal activity (3) and deviant vocal tract events (4) during a stuttering moment may be reflections of this basic organic problem. Secondary aspects of stuttering, such as the severity, are definitely exacerbated by stressful environments. Concomitant behaviors, such as grimaces, eye blinks, and shoulder jerks, may be present as the result of operant learning. About 5% of males and 2% offemales stutter for at least six months sometime during childhood (5), but many affected children recover before they become adults and the adult prevalence is not precisely known. Although stuttering is a common disorder, it has an unknown and probably complex etiology.The probable organic basis and the well-recognized tendency to "run in families" indicate that the etiology of stuttering may have a genetic component. Although there is no simple Mendelian pattern of inheritance, recent analyses have shown that the frequencies of relatives who stutter could be explained by genetic hypotheses. Both polygenic and single-major-locus models have been shown to be compatible with the data (5-9). However, compatibility with two quite different hypotheses cannot be considered strong evidence in favor ofa genetic etiology, nor do any analyses eliminate the possibility ofcultural inheritance. These considerations motivate the use of different analytic approaches. Methods are needed that are not based on etiologic hypotheses but will allow the testing of factors that migh...