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Why and how should we study infant cry?
International Journal of Pediatric Otorhinolaryngology, 24 (1992) 145-159 0 1992 Elsevier Science Publishers B.V. All rights reserved 0165.5876/92/$05.00
PEDOT
145
00808
Why and how should we study infant cry?
’
H.S. Gopal and Sanford E. Gerber Department of Speech and Hearing Sciences, University of California, Santa Barbara, CA (USA) (Revised
Key words: Infant;
Cry; Acoustical
(Received 5 March 1991) version received 25 November (Accepted 29 November 199 I)
1991)
analyses
Abstract
The study of the acoustics of infants’ vocalizations has important implications for the study of infant development and for clinical prediction. We suggest procedures that enhance the probability of discriminating among sub-glottal, periglottal, and supraglottal sites of pathology. With these procedures, then, it should become possible to contribute to diagnosis and therefore to treatment.
Introduction
The general answer to why we should study infant cry, at least one which accords with our view, was stated by Lieberman Ill]: ,/ the biological substrate of human speech involves an interplay between biological mechanisms that have other vegetative functions and neural and anatomical mechanisms have evolved primarily for their role in facilitating human vocal communication”
that appear (p. 29).
to
In the same volume, Boukydis [I] considered crying “to be a gradation of a pre-verbal distress signal” (p. 210). His notion, evidently, is that crying and its perception constitute an interpersonal event. Although this is undoubtedly true, for us it is not the primary reason why we should study infant cry or other vocalizations. For us, the vocalizations of infants are to be studied as phonatory-respiratory events including the necessary neural substrates. As Hollien [7] observed, cries relate to some physiological event or condition as well as to behavioral events or states. What follows is a review of our experience to date and our perspective of what may be accomplished by the analysis of babies’ cries. Correspondence to: H.S. Gopal, Department Santa Barbara, CA 93106-7050, USA. ’ Presented at the Pacific Voice Conference,
of Speech
and Hearing
San Francisco,
1990.
Sciences,
University
of California,
146
Fig. 1. Sagittal sections of different species from domestic dog to adult human. (Source: Jeffrey T. Laitman, The evolution and development of the human upper respiratory tract. In: R.J. Ruben, T.R. van de Water, and E.W. Rubel (Eds.), The Biology of Change in Otolaryngology, Amsterdam: Excerpta Medica. 1986.)
Parry and Quattromani [19] described the cries of infants who have airway obstructions, and then said that radiography and bronchoscopy can confirm the diagnosis. But, crying and other vocalizations are signals which also can be used to evaluate neurorespiratory (and phonatory) function. It is for this reason that there has been so much interest in the cries of high risk newborns (see, e.g., Ref. 26). In fact, we had earlier claimed that evaluation of phonatory behavior “may assist in the identification of.. . neonates who have airway obstruction and/or inadequate neuromotor control of respiration” (Ref. 21, p. 1). One of the most important laws of biology, as we all know, is that ontogeny recapitulates phylogeny. Consider, therefore, Fig. 1 [lo]. Beginning at the upper left and proceeding left to right, we see first the domestic dog (A), the domestic cat (B), spider monkey (0, chimpanzee CD), a newborn human (E), and a 58-year-old human (F). Laitman [lo] pointed out the high position of the larynx and the fact that the epiglottis is in contact with the velum in all specimens except the human
Fig. 2. Premature Pediatric
human infant and adult skulls. (Source: Becky L. McGraw and Randolph R. Cole, maxillofacial trauma, Arch. Otolaryngol. Head Neck Surg., 116 (1990) 41-4.5.)
adult. The phylogeny is evident, but also consider the ontogeny as displayed in Fig. 2 [HI. Observe that the infant’s face is small with respect to head size. Craniofacial ratio decreases from 8: 1 in infancy to 2.5 : 1 in adulthood. These basic anatomical facts must lead us to some acoustical expectations, viz., we need first to examine the acoustics of vocalizations of normal infants. Only with this knowledge can we know if the phonatory output of any given infant is what we would like it to be. Consider the consequences of these anatomical differences. A major characteristic of the adult vocal tract is the right-angle configuration it forms at the craniovertebral junction (refer to Fig. 1). The oral cavity lies along a horizontal axis aligned with the base of the cranium, whereas the pharyngeal and laryngeal cavities are along a vertical axis aligned with the spinal cord. This makes the adult vocal tract a cavity that is sharply bent around the oropharynx. This sharply bent configuration is absent in every other animal species as well as in the human infant. In the infant under six months of age, there is only a gradual bending of the oropharyngeal cavity. The infant configuration is due largely to the fact that the epiglottis is positioned very high in the oropharyngeal tract such that it is in contact with the velum. Additionally, the larynx is also positioned quite high, somewhere around C2 (the second cervical vertebra) position. In contrast, the adult larynx and the epiglottis are positioned much lower, i.e., close to C5. This lowered position of the epiglottis and the larynx provides for much larger oropha-
148
ryngeal and pharyngeal cavities. By adulthood, the epiglottis and the velum are well separated and no longer in contact with each other. The descent of the larynx, which takes place around 4 to 6 months of age [9,21], produces the sharp bending of the vocal tract in the human adult. Knowing why there is this dissimilarity in formation between the adult and the infant, what is the significance of this configurational difference? One major consequence is that this allows for simultaneous feeding and respiration in the infant. Infants have no control over the soft palate; therefore, they are obligatory nose breathers. Because the epiglottis and the velum are juxtaposed, infants can continue to breathe while feeding. The larynx needs to be closed off by the epiglottis only during the brief moments of a swallow. Another major consequence, and a more important one from the standpoint of speech production, is that the lack of control of the velum impacts the repertoire of possible speech sounds. First and foremost, the infant is unable to produce consonant sounds. Production of stops, fricatives and affricates requires sufficient amounts of air pressure in the oral cavity. In the human adult, this is made possible by sealing off the nasal passage and narrowing the constriction through which air flows in the oral cavity. In the infant, a failure to seal the nasal cavity results in a loss of air pressure; therefore, production of most consonants is compromised. Second, the distinction between nasal and non-nasal sounds is lost. Generation of nasal vs. non-nasal sounds requires the ability to control the soft palate at will. Absence of this control renders most vocalic sounds, even vowels, as having a strong nasal component 1891. Thus, the developmental anatomy contributes significantly to the type of speech sounds possible in the human infant. This information is of great benefit to us. First, it tells us that, in normal infants, we would expect primarily vocalic (and nasalized) sounds. In our acoustical analyses of cries, we would expect a large amount of periodicity or regularity when dealing with normal cries, Hence, a great degree of irregularity (or aperiodic&) should warn us that something is amiss, e.g., a lack of normal control, a narrowing of the airway, etc. Secondly, these analyses may provide a way to distinguish between airway obstructions below the nasopharyngeal region from those within the nasopharyngeal space. If normal infants’ cries have a high degree of nasality due to lack of control of the soft palate, absence of such nasality could be an indication of nasal passage obstruction. With this objective in mind, a number of investigators has employed acoustical analyses of various sorts of both normal and non-normal infants [4,12,13,16-18,22251. For example, for over 30 years, several Finnish and Swedish researchers [12,13,16-18,22-251 have used the sound spectrograph and conducted systematic acoustical analyses of cries. They have provided large amounts of acoustical data on cries of normal .infants as well as on cries of several different types of non-normal infants. This vast body of research has provided much of the justification and inspiration for using acoustical analyses of cries as an additional diagnostic tool in clinical pediatrics. More recently, sophisticated and automated computer analyses of cries have been undertaken with the same objective in mind. For example, Golub and Corwin
149
[4], employing sophisticated acoustical techniques, analyzed the cries of 87 infants. They extracted 88 acoustic features and, by a grouping of some combination of these features, they designed a set of eight cry tests which was based on their model of cry production. They reported that a majority of the normal cries (about 82%) had none of the abnormal cry features, whereas the majority of the cries from the non-normal infants evidenced one or more abnormal features. These newer, automated, sophisticated analyses provide increasing promise for cry analysis as a powerful non-invasive tool in the future. However, more studies are needed to establish standardized procedures and templates for acoustical analyses of cries before the true potential of cry analysis may be evaluated and harnessed. To reiterate our emphasis, we first need to examine the acoustics of vocalizations of normal infants in a systematic way. This will help us substantially in understanding the development of speech production as well as our attempts to use infant cry analysis for diagnostic purposes.
Hypotheses
In embarking upon our work on infants’ vocalizations, we established some hypotheses. These hypotheses, in turn, could lead us to some fulfilled wishes. The first hypothesis is that some infants don’t sound like some other infants. This, we trust, is self-evident. Those of us who spend time in newborn nurseries have had the experience of a nurse or other care giver commenting that “that kid doesn’t sound right” or “this one has a funny cry.” They are usually right, but “a funny Cl-f’ is not diagnostically useful. It does tell us, though, that these care givers recognize the cry of a well baby, and know when they heard something else. For us, this means that acoustical analyses of infant cries may help to separate the normal babies from the non-normal ones. The second hypothesis is that this recognizably unusual cry is caused by some disturbance, even abnormality, of respiratory function. This disruption could be due to faulty neural control of respiration (including phonation) as might be produced by Down syndrome, cri du chat syndrome, or damage to the recurrent nerve, inter alia. On the other hand, it could be produced by some disarrangement in the airway itself, for example, tracheostenosis, laryngomalacia, or upper airway abnormality. The third hypothesis is that we should be able to tell the difference between subglottal and supraglottal sites of disruption and tell the difference between airway and nervous system origins by performing acoustical analyses of these cries. The fourth hypothesis - maybe this is the one which is a wish - is that we should eventually be able to come to a state of comprehension such that we could know what is wrong. That is, we hope to arrive at a level of understanding such that we would be able to say confidently that, e.g., “Yes, this is clearly the cry of an infant with choanal atresia,” or “Obviously, this baby has had a lesion of the recurrent nerve”. However, this may be a utopian expectation. The relationship between specific disorders and diseases and their acoustic consequences is not
150
one-to-one. As a minimum, though, we hope to achieve a degree of diagnostic skill that could aid us in inferring whether the disorder is structure-based (extra growth, narrowing of passage etc.) or function-based (paralysis of vocal folds, additional vibrating structures etc.). Moreover, it may aid us in locating the site of lesions periglottal, subglottal or supraglottal.
Work to date
The underlying assumption, obviously, of these hypotheses and of the work so far undertaken is that study of the acoustics of infants’ cries leads to an understanding (or a contribution to it) of the anatomy and/or physiology of what we are calling the neurorespiratory system. So, we began our work with the normal infant. Here, too, we made some rather obvious assumptions. One was that infants cry for reasons other than pain, and it is therefore not necessary to inflict pain on a baby in order to record a cry. Indeed, there are properties of the pain cry that may be diagnostically useful, especially cry latency; we haven’t studied them. A second observation was that an infant has only one vocal tract to use for vocalization and it does not change its structure with different causes of crying. That is, an infant uses the same vocal tract for crying, cooing, burping etc. and for pain cries, hunger cries, discomfort cries etc., although it may be that there are differences in the
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151
Fig. 4. Spectrum
and waveform
section
of normal
infant cry
acoustic properties of these various cries. Fig. 3 [21 shows a one-third-octave band analysis of cry and non-cry sounds averaged over 16 children who ranged in age from 9 to 62 h, who had no Apgar scores lower than 7, and who had no Prechtl [20] score above 2. These data make the point that there are no important differences between non-cry and cry vocalization in the full-term, well newborn. Admittedly, there are more sophisticated techniques than one-third-octave band analysis; nevertheless, we did not evidence any important differences between crying and other phonatory events. We took one baby of the 16 whom we considered to be typical, and did some more analyses. Fig. 4 is the spectrum and a section of the waveform of that baby’s cry, and Fig. 5 is an analysis that corresponds to them but based on linear predictive coding (LPC). The spectrum contains the detailed acoustical information from both the laryngeal source and the resonances of the vocal tract, whereas the LPC analysis primarily captures the vocal tract resonances. So, we believed that we had established a template, if you will, for both the laryngeal and vocal tract acoustic characteristics of a normal cry. Others have employed different analysis techniques including cinefluorography, one-third and one-half octave band analyses, spectrographic analyses, waveform analyses, spectra1 analysis, and even listener transcriptions. So far, we cannot claim any inherent superiority of our technique. But, we are optimistic that a battery of these analysis techniques may help to provide templates for several broad categories of vocalizations in distinguishing between normal and several non-normal cries. Given the kind of template just described, we supposed it possible to compare a cry of any infant to it. Furthermore, if we knew what was wrong with the infant, we could be on the way to developing a template for that particular problem. For example, an acoustical analysis of infants with unilateral vocal fold paralysis ought to reveal the three commonly expected events in such a case: first, two fundamen-
152
FRE@UE!W‘[ HZ1 Fig. 5. LPC (linear predictive coding) analysis of normal cry.
tal frequencies, one for each fold; second, high frequency noise due to turbulent air passage through the glottis because the vocal folds never close in the mid-line; and, third, weak intensity and inadequate variation, of intensity due to lack of complete glottal closure. All of these ought to be revealed by acoustical analyses. Fig. 6 is a display of the spectrum and a section of the waveform of the cry of a l-week-old infant with a unilateral vocal fold paralysis evidently as a consequence
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of a shoulder dystocia [3]. This figure clearly shows the presence of noise throughout the frequency range that is very obvious upon comparison with Fig. 4, the spectrum of a normal baby’s cry. Thus, the presence of noise may become readily evident using an analysis such as the long-term averaged spectrum (LTAS). The two fundamental frequencies may be captured by an analysis of periodicity of the acoustic signal, and there are several procedures for doing so. Lack of intensity variation is shown in Fig. 7, which is a display of the waveform and intensity contour (RMS energy) of the same cry from the infant with vocal fold paralysis. Compare this with Fig. 8, which is the waveform and intensity contour display of the cry of a normal infant. It is obvious that the normal cry has greater and more variable intensity. Although not each and every individual with unilateral vocal fold paralysis manifests these typical findings, a majority of them have some combination of these findings. Indeed, in some instances of unilateral vocal fold paralysis, the normal vocal fold can hyper-adduct (as a compensatory motion) and
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cause a complete closure of the glottis with no turbulent air passage through the glottis. In such cases, the irregularity of the vibration of the two vocal folds may still be detected by acoustical analyses. The point here is that various types of acoustical analyses will reveal at least some of the attributes of a pathological cry. We might want to suppose that this is typical of pathology at the level of the glottis, or we may hope that different glottal pathologies would produce different spectra. We have had the opportunity to do an analysis on what we believe to be the first reported case of diplophonia in a newborn [14]. Figures 9 and 10 display the most important characteristic of the diplophonia in this neonate: two fundamental frequencies. This is readily evident in the narrow band spectrogram (Fig. 9). It is also evident as the modulation rate of the first formant (first peak), and less obviously with the higher formants, on Fig. 10. This modulation rate corresponds to the lower of the two fundamental frequencies. Modulation of formant frequencies gives us two pieces of additional information: (1) the second funda-
Fig. 10. LPC (linear
predictive
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of diplophonia.
mental frequency has an origin above the true glottis as it periodically modulates the already periodic glottal waveform; and (2) because of its much lower fundamental frequency of vibration, it must be a fairly massive structure in relation to the vocal folds. Our acoustical inferences and our two specific expectations were confirmed by indirect laryngoscopy which revealed the vibrations of the aryepiglottic folds, structures more massive than the vocal folds and at a higher position (i.e., supraglottal). Notice, however, the characteristic high-frequency noise associated with vocal fold paralysis is not evident here. This confirms our claim that, at least in this case, we can tell the difference between two kinds of glottal pathology diplophonia and unilateral vocal fold paralysis. Admittedly, diplophonia is not a diagnosis per se; it is an auditory description of voice quality that may be caused by any number of factors including unilateral vocal fold paralysis, unilateral tissue growth, etc. Only future studies employing acoustical analyses of voices with the various pathological conditions resulting in diplophonia may help in evaluating the utility of these techniques for differential diagnoses.
156
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What about sub-glottal pathology? We have also studied a case of tracheostenosis. As is known from the study of anatomy, in the human thorax there is an artery which has no name, hence, the innominate artery. On occasion, this artery has been found to be positioned such that it compresses the trachea. In such a case, a genuine tracheostenosis could result and be exhibited by inspiratory stridor [5]. Acoustical analysis of this case should display that stridor, and it does (Fig. 11). Inspiratory stridor is characterized by noise with a concentration of energy in the lower frequencies. It is not expected in instances where there are upper airway problems nor is it usually expected in cases where the problem is at the level of the glottis [5]. The review of Parry and Quattromani [19] found 12 of 30 children had upper airway obstructions. But, in addition to detection of the site of pathology periglottal vs. subglottal vs. supraglottal - we hope that the analyses will also reveal problems associated with the nature of the pathology. Narrowing of the airway passage (including stenosis) ought to reveal the characteristics of stridor. Irregularity in the periodicity of vibration of the folds may indicate a deficit with neural control of the vibratory structures. Irregularity in periodicity mixed with excessive noise may indicate incomplete closure of the glottis (mass growth on the vocal folds or paralysis). Presence of excessive noise alone (either narrow-band or wide-band) may indicate the presence of obstruction in the passage, e.g., mass growth. Hence, several acoustic features may be associated with the various disorders. Obviously, the success of our approach is dependent on more knowledge of the acoustic properties of normal cries as well as those associated with the various pathologies resulting in non-normal cries. It is thus imperative that such a descriptive cataloging take place first.
The future Looking into our crystal ball, which is indeed a bit cloudy, we foresee the following. It is our intent to build an acoustical ‘library’ of cries recorded from
IS7
TABLE
I
Proposed acoustic parameters in the analysis of infant ~~ocalizations Noise measurements Magnitude of noise in low-frequency region (below 1.5 kHz) Magnitude of noise in mid-frequency region (1.5 to 5 kHz) Magnitude of noise in high-frequency region (above 5 kHz) Presence of noise across all frequencies Formant frequency measurements Stationary vs. varying resonances Durations of resonances Presence of nasal resonances Fundamental frequency measurements Variation of fundamental frequency with time Presence of biphonation Jitter (cycle-to-cycle variation of FO) Average RMS intensity of the periodic component Shimmer (cycle-to-cycle variation of intensity) Presence of noise along with periodicity Duration measurements Duration of cry bursts Duration of inter-cry interval Rate of cry bursts (i.e., number
of cries per second)
normal infants and from infants who have had neurorespiratory disorders diagnosed. With the cries in this library, we hope to develop prototypical acoustical templates of various disorders. This would include LTAS, LPC-based analyses, smoothed log magnitude spectra, intensity contours, and various other acoustical information. Some of the parameters that we propose are listed in Table I (also see Ref. 9) and include the following: concentration of noise in various frequency bands, at least in the low-, mid- and high-frequency regions; some measure of periodicity; a measure of the various resonances of the vocal tract; etc. These templates would be derived from the various acoustical analyses of cries of infants with known neurorespiratory disorders. Then, it could be possible to compare the cry of any given infant to these prototypical acoustical templates in the hope to contribute to diagnosis and therefore to treatment. It is conceivable, in fact, that such a procedure could be automated and employed in newborn nurseries. Finally, this work continues, and we persist in our hope that such a library will be constructed. We hope, also, that we have shown the promise of this kind of work.
Acknowledgement
The authors would have been unable to study the abnormal samples without the contribution of William S. Gibson, Jr., MD of Pennsylvania whose patients they are. His continued enthusiasm underscores our efforts.
158
References 1 Boukydis, C.F.Z., Perception of infant crying as an interpersonal event. In B.M. Lester and C.F.Z. Boukydis (Eds.), Infant Crying. Theoretical and Research Perspectives, Plenum press, New York, 1985. 2 Gerber, SE., Acoustical analyses of neonates’ vocalizations, Int. J. Pediat. Otorhinolaryngol., 10 (1985) l-8. 3 Gerber, S.E., Lynch, C.J. and Gibson, W.S., Jr., The acoustic characteristics of the cry of an infant with unilateral vocal fold paralysis, Intern. J. Pediatr. Otorhinolaryngol., 13 (1987) 1-9. 4 Golub, H.L. and Corwin, M.J. Infant cry: a clue to diagnosis, Pediatrics, 69 (1982) 197-201. 5 Gopal, H.S., Gerber, SE., Marasovich, W.A. and Gibson, W.S., Jr., The acoustics of periglottal pathology, in preparation. 6 Hirschberg, J. and Szende, T., Pathological Cry, Stridor, and Cough in Infants, Akademiai Kiado, Budapest, 1982. 7 Hollien, H., Developmental aspects of neonatal vocalizations. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early Speech, College-Hill Press, Houston, 1980. 8 Kent, R.D., Articulatory-acoustic perspectives on speech development. In R.E. Stark (Ed.), Language Behavior in Infancy and Early Childhood, EIsevier/North-Holland, New York, 1981. 9 Kent, R.D. and Murray, A.D., Acoustic features of infant vocalic utterances at 3, 6 and 9 months, J. Acoust. Sot. Am., 72 (1982) 353-365. 10 Laitman, J.T., The evolution and development of the human upper respiratory tract. In R.J. Ruben, T.R. van de Water, and E.W. Rubel (Eds.), The Biology of Change in Otolaryngology, Excerpta Medica, Amsterdam, 1986. 11 Lieberman, P., The physiology of cry and speech in relation to linguistic behavior. In B.M. Lester and C.F.Z. Boukydis (Eds.), Infant Crying. Theoretical and Research Perspectives, Plenum Press, New York, 1985. 12 Lind, J. (Ed.) Newborn infant cry, Acta Paediatr Scandinavica, 163 (1965) (Suppl.) 1-132. 13 Lind, J., Wasz-Hockert, O., Vuorenski, V. and Valanne, E. The vocalization of a newborn brain-damaged child, Ann. Paediatr. Fenniae, 11 (1965), 32-37. 14 Marasovich, W.A., Gopal, H.S., Gerber, SE. and Gibson, W.S., Jr., Diplophonia in a neonate, paper presented at the annual meeting of the Society for Ear, Nose and Throat Advances in Children, 1989. 15 McGraw, B.L. and Cole, R.R., Pediatric maxillofacial trauma, Arch. Otolaryngol. Head Neck Surg., 6 (1990) 41-45. 16 Michelsson, K. Cry analysis of symptomless low birth weight infants and of asphyxiated newborn infants, Acta Paediatr. Stand., 216 (1971) l-45. 17 Michelsson, K. Cry characteristics in sound spectrographic cry analysis. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early Speech, Houston: College-Hill Press, 1980. 18 Michelsson, K. and Wasz-Hiickert, 0. The value of cry analysis in neonatology and early infancy. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early speech, Houston: College-Hill Press, 1980. 19 Parry, W.H. and Quattromani, F., Airway obstruction in the neonate, Perinatol.-Neonatol., 7 (1983) 59-60, 62-63. 20 Prechtl, H.F.R., Neurological findings in newborn infants after pre- and perinatal complications. In J. Jonix, H. Visser and J. Troelstra (Eds.), Aspects of Prematurity and Dysmaturity, Stenfert Korese, Leiden, 1968. 21 Sasaki, C.T., Levine, P.A., Laitman, J.T. and Crelin, E.S., Postnatal descent of the epiglottis in man, Arch. Otolaryngol., 103 (1977) 169-171. 22 Thoden, C.J. and Koivisto, M. Acoustic analysis of the normal pain cry. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early Speech, Houston: College-Hill Press, 1980. 23 Vuorenkoski, V., Lind, J., Partanen, T.J., Lejeune, J., Lafourcade, J. and Wasz-Hiickert, 0. Spectrographic analysis of cries from children with maladie du cri du chat. Ann. Paediatr. Fenniae, 12 (1966) 174-180.
24 Wasz-Hockert, O., Lind, J., Vuorenkoski, V., Valanne, E. and Michelsson, K., Sound spectrographic analysis of the infant cry (in German), Experientia, 18 (1962), 583-586. 25 Wasz-Hockert, O., Vuorenkoski, V., Partanen, T. and Valanne, E. The infant cry: a spectrographic and auditory analysis. Clinics in Developmental Medicine 20. Lavenham, Suffolk: Spastics International Medical Publications, 1968. 26 Zeskind, P.S., Production and spectral analysis of neonatal crying and its relation to other biobehavioral systems in the infant at risk. In T. Field and A. Sostek (Eds.). infants Born at Risk. Grune Rr Stratton, New York, 1983.
PEDOT
145
00808
Why and how should we study infant cry?
’
H.S. Gopal and Sanford E. Gerber Department of Speech and Hearing Sciences, University of California, Santa Barbara, CA (USA) (Revised
Key words: Infant;
Cry; Acoustical
(Received 5 March 1991) version received 25 November (Accepted 29 November 199 I)
1991)
analyses
Abstract
The study of the acoustics of infants’ vocalizations has important implications for the study of infant development and for clinical prediction. We suggest procedures that enhance the probability of discriminating among sub-glottal, periglottal, and supraglottal sites of pathology. With these procedures, then, it should become possible to contribute to diagnosis and therefore to treatment.
Introduction
The general answer to why we should study infant cry, at least one which accords with our view, was stated by Lieberman Ill]: ,/ the biological substrate of human speech involves an interplay between biological mechanisms that have other vegetative functions and neural and anatomical mechanisms have evolved primarily for their role in facilitating human vocal communication”
that appear (p. 29).
to
In the same volume, Boukydis [I] considered crying “to be a gradation of a pre-verbal distress signal” (p. 210). His notion, evidently, is that crying and its perception constitute an interpersonal event. Although this is undoubtedly true, for us it is not the primary reason why we should study infant cry or other vocalizations. For us, the vocalizations of infants are to be studied as phonatory-respiratory events including the necessary neural substrates. As Hollien [7] observed, cries relate to some physiological event or condition as well as to behavioral events or states. What follows is a review of our experience to date and our perspective of what may be accomplished by the analysis of babies’ cries. Correspondence to: H.S. Gopal, Department Santa Barbara, CA 93106-7050, USA. ’ Presented at the Pacific Voice Conference,
of Speech
and Hearing
San Francisco,
1990.
Sciences,
University
of California,
146
Fig. 1. Sagittal sections of different species from domestic dog to adult human. (Source: Jeffrey T. Laitman, The evolution and development of the human upper respiratory tract. In: R.J. Ruben, T.R. van de Water, and E.W. Rubel (Eds.), The Biology of Change in Otolaryngology, Amsterdam: Excerpta Medica. 1986.)
Parry and Quattromani [19] described the cries of infants who have airway obstructions, and then said that radiography and bronchoscopy can confirm the diagnosis. But, crying and other vocalizations are signals which also can be used to evaluate neurorespiratory (and phonatory) function. It is for this reason that there has been so much interest in the cries of high risk newborns (see, e.g., Ref. 26). In fact, we had earlier claimed that evaluation of phonatory behavior “may assist in the identification of.. . neonates who have airway obstruction and/or inadequate neuromotor control of respiration” (Ref. 21, p. 1). One of the most important laws of biology, as we all know, is that ontogeny recapitulates phylogeny. Consider, therefore, Fig. 1 [lo]. Beginning at the upper left and proceeding left to right, we see first the domestic dog (A), the domestic cat (B), spider monkey (0, chimpanzee CD), a newborn human (E), and a 58-year-old human (F). Laitman [lo] pointed out the high position of the larynx and the fact that the epiglottis is in contact with the velum in all specimens except the human
Fig. 2. Premature Pediatric
human infant and adult skulls. (Source: Becky L. McGraw and Randolph R. Cole, maxillofacial trauma, Arch. Otolaryngol. Head Neck Surg., 116 (1990) 41-4.5.)
adult. The phylogeny is evident, but also consider the ontogeny as displayed in Fig. 2 [HI. Observe that the infant’s face is small with respect to head size. Craniofacial ratio decreases from 8: 1 in infancy to 2.5 : 1 in adulthood. These basic anatomical facts must lead us to some acoustical expectations, viz., we need first to examine the acoustics of vocalizations of normal infants. Only with this knowledge can we know if the phonatory output of any given infant is what we would like it to be. Consider the consequences of these anatomical differences. A major characteristic of the adult vocal tract is the right-angle configuration it forms at the craniovertebral junction (refer to Fig. 1). The oral cavity lies along a horizontal axis aligned with the base of the cranium, whereas the pharyngeal and laryngeal cavities are along a vertical axis aligned with the spinal cord. This makes the adult vocal tract a cavity that is sharply bent around the oropharynx. This sharply bent configuration is absent in every other animal species as well as in the human infant. In the infant under six months of age, there is only a gradual bending of the oropharyngeal cavity. The infant configuration is due largely to the fact that the epiglottis is positioned very high in the oropharyngeal tract such that it is in contact with the velum. Additionally, the larynx is also positioned quite high, somewhere around C2 (the second cervical vertebra) position. In contrast, the adult larynx and the epiglottis are positioned much lower, i.e., close to C5. This lowered position of the epiglottis and the larynx provides for much larger oropha-
148
ryngeal and pharyngeal cavities. By adulthood, the epiglottis and the velum are well separated and no longer in contact with each other. The descent of the larynx, which takes place around 4 to 6 months of age [9,21], produces the sharp bending of the vocal tract in the human adult. Knowing why there is this dissimilarity in formation between the adult and the infant, what is the significance of this configurational difference? One major consequence is that this allows for simultaneous feeding and respiration in the infant. Infants have no control over the soft palate; therefore, they are obligatory nose breathers. Because the epiglottis and the velum are juxtaposed, infants can continue to breathe while feeding. The larynx needs to be closed off by the epiglottis only during the brief moments of a swallow. Another major consequence, and a more important one from the standpoint of speech production, is that the lack of control of the velum impacts the repertoire of possible speech sounds. First and foremost, the infant is unable to produce consonant sounds. Production of stops, fricatives and affricates requires sufficient amounts of air pressure in the oral cavity. In the human adult, this is made possible by sealing off the nasal passage and narrowing the constriction through which air flows in the oral cavity. In the infant, a failure to seal the nasal cavity results in a loss of air pressure; therefore, production of most consonants is compromised. Second, the distinction between nasal and non-nasal sounds is lost. Generation of nasal vs. non-nasal sounds requires the ability to control the soft palate at will. Absence of this control renders most vocalic sounds, even vowels, as having a strong nasal component 1891. Thus, the developmental anatomy contributes significantly to the type of speech sounds possible in the human infant. This information is of great benefit to us. First, it tells us that, in normal infants, we would expect primarily vocalic (and nasalized) sounds. In our acoustical analyses of cries, we would expect a large amount of periodicity or regularity when dealing with normal cries, Hence, a great degree of irregularity (or aperiodic&) should warn us that something is amiss, e.g., a lack of normal control, a narrowing of the airway, etc. Secondly, these analyses may provide a way to distinguish between airway obstructions below the nasopharyngeal region from those within the nasopharyngeal space. If normal infants’ cries have a high degree of nasality due to lack of control of the soft palate, absence of such nasality could be an indication of nasal passage obstruction. With this objective in mind, a number of investigators has employed acoustical analyses of various sorts of both normal and non-normal infants [4,12,13,16-18,22251. For example, for over 30 years, several Finnish and Swedish researchers [12,13,16-18,22-251 have used the sound spectrograph and conducted systematic acoustical analyses of cries. They have provided large amounts of acoustical data on cries of normal .infants as well as on cries of several different types of non-normal infants. This vast body of research has provided much of the justification and inspiration for using acoustical analyses of cries as an additional diagnostic tool in clinical pediatrics. More recently, sophisticated and automated computer analyses of cries have been undertaken with the same objective in mind. For example, Golub and Corwin
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[4], employing sophisticated acoustical techniques, analyzed the cries of 87 infants. They extracted 88 acoustic features and, by a grouping of some combination of these features, they designed a set of eight cry tests which was based on their model of cry production. They reported that a majority of the normal cries (about 82%) had none of the abnormal cry features, whereas the majority of the cries from the non-normal infants evidenced one or more abnormal features. These newer, automated, sophisticated analyses provide increasing promise for cry analysis as a powerful non-invasive tool in the future. However, more studies are needed to establish standardized procedures and templates for acoustical analyses of cries before the true potential of cry analysis may be evaluated and harnessed. To reiterate our emphasis, we first need to examine the acoustics of vocalizations of normal infants in a systematic way. This will help us substantially in understanding the development of speech production as well as our attempts to use infant cry analysis for diagnostic purposes.
Hypotheses
In embarking upon our work on infants’ vocalizations, we established some hypotheses. These hypotheses, in turn, could lead us to some fulfilled wishes. The first hypothesis is that some infants don’t sound like some other infants. This, we trust, is self-evident. Those of us who spend time in newborn nurseries have had the experience of a nurse or other care giver commenting that “that kid doesn’t sound right” or “this one has a funny cry.” They are usually right, but “a funny Cl-f’ is not diagnostically useful. It does tell us, though, that these care givers recognize the cry of a well baby, and know when they heard something else. For us, this means that acoustical analyses of infant cries may help to separate the normal babies from the non-normal ones. The second hypothesis is that this recognizably unusual cry is caused by some disturbance, even abnormality, of respiratory function. This disruption could be due to faulty neural control of respiration (including phonation) as might be produced by Down syndrome, cri du chat syndrome, or damage to the recurrent nerve, inter alia. On the other hand, it could be produced by some disarrangement in the airway itself, for example, tracheostenosis, laryngomalacia, or upper airway abnormality. The third hypothesis is that we should be able to tell the difference between subglottal and supraglottal sites of disruption and tell the difference between airway and nervous system origins by performing acoustical analyses of these cries. The fourth hypothesis - maybe this is the one which is a wish - is that we should eventually be able to come to a state of comprehension such that we could know what is wrong. That is, we hope to arrive at a level of understanding such that we would be able to say confidently that, e.g., “Yes, this is clearly the cry of an infant with choanal atresia,” or “Obviously, this baby has had a lesion of the recurrent nerve”. However, this may be a utopian expectation. The relationship between specific disorders and diseases and their acoustic consequences is not
150
one-to-one. As a minimum, though, we hope to achieve a degree of diagnostic skill that could aid us in inferring whether the disorder is structure-based (extra growth, narrowing of passage etc.) or function-based (paralysis of vocal folds, additional vibrating structures etc.). Moreover, it may aid us in locating the site of lesions periglottal, subglottal or supraglottal.
Work to date
The underlying assumption, obviously, of these hypotheses and of the work so far undertaken is that study of the acoustics of infants’ cries leads to an understanding (or a contribution to it) of the anatomy and/or physiology of what we are calling the neurorespiratory system. So, we began our work with the normal infant. Here, too, we made some rather obvious assumptions. One was that infants cry for reasons other than pain, and it is therefore not necessary to inflict pain on a baby in order to record a cry. Indeed, there are properties of the pain cry that may be diagnostically useful, especially cry latency; we haven’t studied them. A second observation was that an infant has only one vocal tract to use for vocalization and it does not change its structure with different causes of crying. That is, an infant uses the same vocal tract for crying, cooing, burping etc. and for pain cries, hunger cries, discomfort cries etc., although it may be that there are differences in the
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acoustic properties of these various cries. Fig. 3 [21 shows a one-third-octave band analysis of cry and non-cry sounds averaged over 16 children who ranged in age from 9 to 62 h, who had no Apgar scores lower than 7, and who had no Prechtl [20] score above 2. These data make the point that there are no important differences between non-cry and cry vocalization in the full-term, well newborn. Admittedly, there are more sophisticated techniques than one-third-octave band analysis; nevertheless, we did not evidence any important differences between crying and other phonatory events. We took one baby of the 16 whom we considered to be typical, and did some more analyses. Fig. 4 is the spectrum and a section of the waveform of that baby’s cry, and Fig. 5 is an analysis that corresponds to them but based on linear predictive coding (LPC). The spectrum contains the detailed acoustical information from both the laryngeal source and the resonances of the vocal tract, whereas the LPC analysis primarily captures the vocal tract resonances. So, we believed that we had established a template, if you will, for both the laryngeal and vocal tract acoustic characteristics of a normal cry. Others have employed different analysis techniques including cinefluorography, one-third and one-half octave band analyses, spectrographic analyses, waveform analyses, spectra1 analysis, and even listener transcriptions. So far, we cannot claim any inherent superiority of our technique. But, we are optimistic that a battery of these analysis techniques may help to provide templates for several broad categories of vocalizations in distinguishing between normal and several non-normal cries. Given the kind of template just described, we supposed it possible to compare a cry of any infant to it. Furthermore, if we knew what was wrong with the infant, we could be on the way to developing a template for that particular problem. For example, an acoustical analysis of infants with unilateral vocal fold paralysis ought to reveal the three commonly expected events in such a case: first, two fundamen-
152
FRE@UE!W‘[ HZ1 Fig. 5. LPC (linear predictive coding) analysis of normal cry.
tal frequencies, one for each fold; second, high frequency noise due to turbulent air passage through the glottis because the vocal folds never close in the mid-line; and, third, weak intensity and inadequate variation, of intensity due to lack of complete glottal closure. All of these ought to be revealed by acoustical analyses. Fig. 6 is a display of the spectrum and a section of the waveform of the cry of a l-week-old infant with a unilateral vocal fold paralysis evidently as a consequence
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of a shoulder dystocia [3]. This figure clearly shows the presence of noise throughout the frequency range that is very obvious upon comparison with Fig. 4, the spectrum of a normal baby’s cry. Thus, the presence of noise may become readily evident using an analysis such as the long-term averaged spectrum (LTAS). The two fundamental frequencies may be captured by an analysis of periodicity of the acoustic signal, and there are several procedures for doing so. Lack of intensity variation is shown in Fig. 7, which is a display of the waveform and intensity contour (RMS energy) of the same cry from the infant with vocal fold paralysis. Compare this with Fig. 8, which is the waveform and intensity contour display of the cry of a normal infant. It is obvious that the normal cry has greater and more variable intensity. Although not each and every individual with unilateral vocal fold paralysis manifests these typical findings, a majority of them have some combination of these findings. Indeed, in some instances of unilateral vocal fold paralysis, the normal vocal fold can hyper-adduct (as a compensatory motion) and
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cause a complete closure of the glottis with no turbulent air passage through the glottis. In such cases, the irregularity of the vibration of the two vocal folds may still be detected by acoustical analyses. The point here is that various types of acoustical analyses will reveal at least some of the attributes of a pathological cry. We might want to suppose that this is typical of pathology at the level of the glottis, or we may hope that different glottal pathologies would produce different spectra. We have had the opportunity to do an analysis on what we believe to be the first reported case of diplophonia in a newborn [14]. Figures 9 and 10 display the most important characteristic of the diplophonia in this neonate: two fundamental frequencies. This is readily evident in the narrow band spectrogram (Fig. 9). It is also evident as the modulation rate of the first formant (first peak), and less obviously with the higher formants, on Fig. 10. This modulation rate corresponds to the lower of the two fundamental frequencies. Modulation of formant frequencies gives us two pieces of additional information: (1) the second funda-
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mental frequency has an origin above the true glottis as it periodically modulates the already periodic glottal waveform; and (2) because of its much lower fundamental frequency of vibration, it must be a fairly massive structure in relation to the vocal folds. Our acoustical inferences and our two specific expectations were confirmed by indirect laryngoscopy which revealed the vibrations of the aryepiglottic folds, structures more massive than the vocal folds and at a higher position (i.e., supraglottal). Notice, however, the characteristic high-frequency noise associated with vocal fold paralysis is not evident here. This confirms our claim that, at least in this case, we can tell the difference between two kinds of glottal pathology diplophonia and unilateral vocal fold paralysis. Admittedly, diplophonia is not a diagnosis per se; it is an auditory description of voice quality that may be caused by any number of factors including unilateral vocal fold paralysis, unilateral tissue growth, etc. Only future studies employing acoustical analyses of voices with the various pathological conditions resulting in diplophonia may help in evaluating the utility of these techniques for differential diagnoses.
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What about sub-glottal pathology? We have also studied a case of tracheostenosis. As is known from the study of anatomy, in the human thorax there is an artery which has no name, hence, the innominate artery. On occasion, this artery has been found to be positioned such that it compresses the trachea. In such a case, a genuine tracheostenosis could result and be exhibited by inspiratory stridor [5]. Acoustical analysis of this case should display that stridor, and it does (Fig. 11). Inspiratory stridor is characterized by noise with a concentration of energy in the lower frequencies. It is not expected in instances where there are upper airway problems nor is it usually expected in cases where the problem is at the level of the glottis [5]. The review of Parry and Quattromani [19] found 12 of 30 children had upper airway obstructions. But, in addition to detection of the site of pathology periglottal vs. subglottal vs. supraglottal - we hope that the analyses will also reveal problems associated with the nature of the pathology. Narrowing of the airway passage (including stenosis) ought to reveal the characteristics of stridor. Irregularity in the periodicity of vibration of the folds may indicate a deficit with neural control of the vibratory structures. Irregularity in periodicity mixed with excessive noise may indicate incomplete closure of the glottis (mass growth on the vocal folds or paralysis). Presence of excessive noise alone (either narrow-band or wide-band) may indicate the presence of obstruction in the passage, e.g., mass growth. Hence, several acoustic features may be associated with the various disorders. Obviously, the success of our approach is dependent on more knowledge of the acoustic properties of normal cries as well as those associated with the various pathologies resulting in non-normal cries. It is thus imperative that such a descriptive cataloging take place first.
The future Looking into our crystal ball, which is indeed a bit cloudy, we foresee the following. It is our intent to build an acoustical ‘library’ of cries recorded from
IS7
TABLE
I
Proposed acoustic parameters in the analysis of infant ~~ocalizations Noise measurements Magnitude of noise in low-frequency region (below 1.5 kHz) Magnitude of noise in mid-frequency region (1.5 to 5 kHz) Magnitude of noise in high-frequency region (above 5 kHz) Presence of noise across all frequencies Formant frequency measurements Stationary vs. varying resonances Durations of resonances Presence of nasal resonances Fundamental frequency measurements Variation of fundamental frequency with time Presence of biphonation Jitter (cycle-to-cycle variation of FO) Average RMS intensity of the periodic component Shimmer (cycle-to-cycle variation of intensity) Presence of noise along with periodicity Duration measurements Duration of cry bursts Duration of inter-cry interval Rate of cry bursts (i.e., number
of cries per second)
normal infants and from infants who have had neurorespiratory disorders diagnosed. With the cries in this library, we hope to develop prototypical acoustical templates of various disorders. This would include LTAS, LPC-based analyses, smoothed log magnitude spectra, intensity contours, and various other acoustical information. Some of the parameters that we propose are listed in Table I (also see Ref. 9) and include the following: concentration of noise in various frequency bands, at least in the low-, mid- and high-frequency regions; some measure of periodicity; a measure of the various resonances of the vocal tract; etc. These templates would be derived from the various acoustical analyses of cries of infants with known neurorespiratory disorders. Then, it could be possible to compare the cry of any given infant to these prototypical acoustical templates in the hope to contribute to diagnosis and therefore to treatment. It is conceivable, in fact, that such a procedure could be automated and employed in newborn nurseries. Finally, this work continues, and we persist in our hope that such a library will be constructed. We hope, also, that we have shown the promise of this kind of work.
Acknowledgement
The authors would have been unable to study the abnormal samples without the contribution of William S. Gibson, Jr., MD of Pennsylvania whose patients they are. His continued enthusiasm underscores our efforts.
158
References 1 Boukydis, C.F.Z., Perception of infant crying as an interpersonal event. In B.M. Lester and C.F.Z. Boukydis (Eds.), Infant Crying. Theoretical and Research Perspectives, Plenum press, New York, 1985. 2 Gerber, SE., Acoustical analyses of neonates’ vocalizations, Int. J. Pediat. Otorhinolaryngol., 10 (1985) l-8. 3 Gerber, S.E., Lynch, C.J. and Gibson, W.S., Jr., The acoustic characteristics of the cry of an infant with unilateral vocal fold paralysis, Intern. J. Pediatr. Otorhinolaryngol., 13 (1987) 1-9. 4 Golub, H.L. and Corwin, M.J. Infant cry: a clue to diagnosis, Pediatrics, 69 (1982) 197-201. 5 Gopal, H.S., Gerber, SE., Marasovich, W.A. and Gibson, W.S., Jr., The acoustics of periglottal pathology, in preparation. 6 Hirschberg, J. and Szende, T., Pathological Cry, Stridor, and Cough in Infants, Akademiai Kiado, Budapest, 1982. 7 Hollien, H., Developmental aspects of neonatal vocalizations. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early Speech, College-Hill Press, Houston, 1980. 8 Kent, R.D., Articulatory-acoustic perspectives on speech development. In R.E. Stark (Ed.), Language Behavior in Infancy and Early Childhood, EIsevier/North-Holland, New York, 1981. 9 Kent, R.D. and Murray, A.D., Acoustic features of infant vocalic utterances at 3, 6 and 9 months, J. Acoust. Sot. Am., 72 (1982) 353-365. 10 Laitman, J.T., The evolution and development of the human upper respiratory tract. In R.J. Ruben, T.R. van de Water, and E.W. Rubel (Eds.), The Biology of Change in Otolaryngology, Excerpta Medica, Amsterdam, 1986. 11 Lieberman, P., The physiology of cry and speech in relation to linguistic behavior. In B.M. Lester and C.F.Z. Boukydis (Eds.), Infant Crying. Theoretical and Research Perspectives, Plenum Press, New York, 1985. 12 Lind, J. (Ed.) Newborn infant cry, Acta Paediatr Scandinavica, 163 (1965) (Suppl.) 1-132. 13 Lind, J., Wasz-Hockert, O., Vuorenski, V. and Valanne, E. The vocalization of a newborn brain-damaged child, Ann. Paediatr. Fenniae, 11 (1965), 32-37. 14 Marasovich, W.A., Gopal, H.S., Gerber, SE. and Gibson, W.S., Jr., Diplophonia in a neonate, paper presented at the annual meeting of the Society for Ear, Nose and Throat Advances in Children, 1989. 15 McGraw, B.L. and Cole, R.R., Pediatric maxillofacial trauma, Arch. Otolaryngol. Head Neck Surg., 6 (1990) 41-45. 16 Michelsson, K. Cry analysis of symptomless low birth weight infants and of asphyxiated newborn infants, Acta Paediatr. Stand., 216 (1971) l-45. 17 Michelsson, K. Cry characteristics in sound spectrographic cry analysis. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early Speech, Houston: College-Hill Press, 1980. 18 Michelsson, K. and Wasz-Hiickert, 0. The value of cry analysis in neonatology and early infancy. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early speech, Houston: College-Hill Press, 1980. 19 Parry, W.H. and Quattromani, F., Airway obstruction in the neonate, Perinatol.-Neonatol., 7 (1983) 59-60, 62-63. 20 Prechtl, H.F.R., Neurological findings in newborn infants after pre- and perinatal complications. In J. Jonix, H. Visser and J. Troelstra (Eds.), Aspects of Prematurity and Dysmaturity, Stenfert Korese, Leiden, 1968. 21 Sasaki, C.T., Levine, P.A., Laitman, J.T. and Crelin, E.S., Postnatal descent of the epiglottis in man, Arch. Otolaryngol., 103 (1977) 169-171. 22 Thoden, C.J. and Koivisto, M. Acoustic analysis of the normal pain cry. In T. Murry and J. Murry (Eds.), Infant Communication: Cry and Early Speech, Houston: College-Hill Press, 1980. 23 Vuorenkoski, V., Lind, J., Partanen, T.J., Lejeune, J., Lafourcade, J. and Wasz-Hiickert, 0. Spectrographic analysis of cries from children with maladie du cri du chat. Ann. Paediatr. Fenniae, 12 (1966) 174-180.
24 Wasz-Hockert, O., Lind, J., Vuorenkoski, V., Valanne, E. and Michelsson, K., Sound spectrographic analysis of the infant cry (in German), Experientia, 18 (1962), 583-586. 25 Wasz-Hockert, O., Vuorenkoski, V., Partanen, T. and Valanne, E. The infant cry: a spectrographic and auditory analysis. Clinics in Developmental Medicine 20. Lavenham, Suffolk: Spastics International Medical Publications, 1968. 26 Zeskind, P.S., Production and spectral analysis of neonatal crying and its relation to other biobehavioral systems in the infant at risk. In T. Field and A. Sostek (Eds.). infants Born at Risk. Grune Rr Stratton, New York, 1983.