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Changing Our Understanding of Infant Colic  Ronald
G. Barr, MDCM, FRCPC COLIC IS truly a noisy phenomenon in terms of the crying that the infant does. But it is also a noisy phenomenon to study in terms of the basic phenomenonology of crying that constitutes the defining behavioral feature of the syndrome. As can be appreciated in Figure 3 in the article by Clifford et al 1 in this issue of the ARCHIVES, even at 3 months of age, after most colic has resolved, there is still a substantial range of minutes per week (or per day) of crying and fussing behavior. This is also true in the sixth week of life, when crying is usually manifest at its highest levels.2-4 In addition to the range of "individual differences" in levels of crying among infants, there is no single level of crying in early infancy that is normative.5 Indeed, the total number of minutes of daily distress manifest an n-shaped pattern over the first 3 months or so of life: they begin to increase at about 2 weeks of age, peak during the sixth week, and then decline to under 1 h/d by 12 weeks of age. While this pattern is typical for groups of infants, individual infants may experience their maximum distress at earlier or later ages so that a single measure at a particular age may not capture the maximum for that infant (see Figure 2, Barr4).All of this has made early crying and its main clinical manifestation of colic difficult to study. Nevertheless, an increasing number of studies with a variety of designs has brought some degree of "order"6 to this noisy phenomenon. Among the themes emerging from these findings are that (1) the n-shaped (or "peak") pattern of crying, long thought to be the defining characteristic of the clinical syndrome of colic, is now understood to be a likely behavioral universal of normal infant development in the sense that human infants share a propensity for increased crying that is characteristic of all groups of infants in the human species, if not of all infants6; (2) probably all of the other defining features of the syndrome can also be accounted for without positing any pathophysiological process or abnormality in most infants with colic7, 8; (3) the levels of crying variously and variably described as defining characteristics of colic syndrome9, 10 reflect in most cases the upper end of the spectrum of early developmental crying behavior, such that the prevalence varies depending on the time of measurement and the cut-off value of daily distress used; (4) despite its name that suggests gastrointestinal tract problems, the prolonged crying episodes may well be related to individual differences in central nervous system functioning rather than gastrointestinal tract dysfunction8, 11-13; and (5) the outcome for infants with colic is good, at least in low-risk populations and in the absence of significant comorbidity or stress in the infant and/or parents (see Clifford et al1 and others14). None of the above is inconsistent with there being some infants with significant disease or pathophysiological processes, or with abnormal cries or amounts of crying, being included in the group of infants who meet clinical criteria of colic.15, 16 Nor is it inconsistent with there being increased crying in mother-infant dyads in which the normal coregulatory interactions that modify the infant behavioral state have broken down.17, 18 Furthermore, it remains possible, if still hypothetical, that the source of the disturbance could be situated in the gastrointestinal tract even in the absence of disease processes if the crying reflects visceral hypersensivity to otherwise innocuous intestinal stimuli.19 This would be the infant analogue of the processes of "hyperalgesia" (which refers to a reduced pain threshold or a greater or longer duration of response to a painful stimulus) and "allodynia" (which is when painful or discomforting experiences are due to stimuli that do not normally produce pain or discomfort) in adults. If one follows this hypothesis, the hypersensitivity occurs when there are changes in the sensitivities of the primary afferent neurons or in secondary dorsal horn neurons.20, 21 The fact that local interneuronal inhibitory connections in the substantia gelatinosa and the descending inhibition ("gating") from the brainstem on dorsal horn cells are all postnatal events (in the rat and probably in humans) might account for the decrease in crying during the third month owing to this mechanism.22 In short, the new information about the normative developmental crying pattern has not solved the clinical problem of infant colic; rather, it has provided important basic information against which these other processes now need to be assessed with regard to diagnosis, therapy, and prognosis. The article by Clifford and colleagues1 in this issue is the latest of the still too few prospective studies of infant colic in which, importantly, there was some means of measuring infant colic when it occurred, rather than depending on parent recall.14 They report a number of important observations, including the prevalence of levels of crying consistent with colic at age 3 months (6.4%), and that 85% of cases with colic remitted by age 3 months. They also report that, at least in this relatively low-risk population, (trait) anxiety and postnatal depression are not elevated in the mothers of infants who previously had colic. Importantly, this was assessed with control measures of anxiety and depression at 1 week post partum, a methodological strength of this study missing in most others (but see also Murray and Cooper23). To my mind, by far the most intriguing observation is not even mentioned in the abstract and may turn out to be the most important one for our future understanding of this syndrome. This is the documentation of the fact that of the 6.4% of infants who met criteria for colic at age 3 months, only about half of those met criteria for colic at 6 weeks and at 3 months of age (which they called "persistent" cases) and the other half did not meet criteria for colic at 6 weeks but did at 3 months of age (which they called "latent" cases). There are a number of reasons why this observation may be particularly prescient. One reason is that it has been thought for some time that, in the absence of pathology, infant colic is the earliest manifestation of later "difficult" temperament. Although temperament caregiver report measures taken when the infant has colic always confirm one or other form of "difficultness,"24, 25 prospective longitudinal studies do not support this hypothesis (see especially Lehtonen et al26 as well as a review of this evidence by Barr and Gunnar24). The question is, if infants with prior colic do not become infants with difficult temperaments later, which ones do? One possibility, counterintuitive though it may be, is that infants with difficult temperaments actually tend to be those who do not have colic early, but whose difficultness emerges after the early 3-month period, or following what is sometimes referred to as the "biobehavioral shift."27 Barr and Gunnar24 have incorporated such a speculation in their "transient responsivity hypothesis" about infant colic. They argue not only that infants with colic are as well regulated as infants without, but that they may even be better regulated later. Although intriguing, the evidence for this is still very weak. If Clifford and colleagues decide to do a follow-up study on these infants (as they have promised), they may be able to address this speculation empirically. A second reason is this. Mechthild Papousek and her colleagues17,
18, 28, 29
have been carefully documenting for some time the interactional breakdowns
that occur between constantly crying infants and their caregivers in the
first year of life who present to their exceptional clinic in Munich,
Germany. A proportion of their patients clearly have prior colic with crying
that continues. However, they also tend to be "high risk" in the sense that
there are also disturbances in feeding and/or sleeping, mild developmental
delays, and organic risk factors In their discussion, Clifford and colleagues comment that the relatively
good prognosis they describe "should not justify the abandonment of
research."1(pswk) Indeed, not. More research is
critical even if (as I and others have argued elsewhere7,
8, 31) the n-shaped curve of
early infant crying with its large interindividual differences and
accompanying prolonged episodes of unsoothable, painful-appearing distress
are a manifestation of typical behavioral development, probably an
inheritance from our evolutionary history
The author acknowledges the McGill University Chair in Child Development fund, Montreal, Quebec, for support of the writing of this commentary.
REFERENCES
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© 2002 American Medical Association. All rights reserved. |
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a
group that has been dubbed the "persistent mother-infant distress" syndrome
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