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Infantile colic as the clinical expression of
brainstem dysregulation: a narrative review
Jan Hoeve, PhD, DC
Chiropractie Staphorst, The Netherlands
janhoeve@chiropractiestaphorst.nl
ABSTRACT
Despite many years of research, the cause of
infantile colic is as elusive as ever and no
distinct cure has emerged. Evidence is reviewed
that colic may be the clinical expression of
physiological dysregulation at the brainstem
level, particularly of the vestibular and
autonomic systems. It is argued that
occipital/upper-cervical muscular tightness
acquired at birth may induce aberrant
proprioceptive flow into the vestibular system
and, indirectly, the medial cerebellar cortex.
Diminished inhibitory modulation of the
vestibular nuclei by the medial cerebellum may
provide a mechanism of how vestibular
dysregulation/ hyperactivity may arise and
subsequently be propagated downstream to also
involve the autonomic systems. Treatment aimed
at relaxation of tight sub-occipital musculature
may restore regular proprioceptive flow and
facilitate normalization of the inhibitory
cerebellar modulation of the vestibular nuclei.
From an evolutionary perspective the high
prevalence of infantile colic may be an inherent
aspect of the human condition and may be the
price we pay for our upright stance, bipedal
gait and difficult birth process as compared to
the great apes. The focus of future research
should be broadened to include the concomitant
symptoms of colic that point to brainstem
involvement.
Key Words: Infantile colic,
brainstem dysregulation, sub-occipital
dysfunction, proprioception, sensory
neuromodulation, vestibular, autonomic.
Introduction
With an estimated prevalence of 15-25% infantile
colic is one of the commonest early childhood
afflictions, along with Functional
Gastro-Intestinal Disorders (FGID)1,2
Still, colic remains enigmatic. To date, 68
years after the rule-of-three diagnostic
criteria were formulated3 and after a
great deal of research, the cause of colic is as
elusive as ever and no distinct cure has
emerged. In the intervening years much research
has been focused on the crying per se and on
establishing if and how colicky crying differs
from normal crying2,4 In addition, a
multitude of possible contributing factors,
pathological and non-pathological, have been
proposed, often in a rather haphazard fashion.
These include dietary causes such as cow’s milk
or fructose intolerance, GER(D),
(neuro)developmental problems, behavioral
problems, difficult temperament, transient
hyperresponsivity, immaturity of the gut, gut
dysbiosis, over/ underfeeding, imbalance of the
autonomic nervous system, high levels of
distress.5-7 Organic pathology is
rarely present.8 Several authors have
suggested that colic is just the extreme end of
a spectrum of normal crying behavior,9,10
although this is unlikely from an evolutionary
as well as an energy perspective.11
Others pointed to the dynamics of infant-parent
interaction.12 This is also unlikely
as it cannot account for those cases where one
baby of a pair of twins is colicky whereas the
other is not.11 In recent years a
close association with childhood/adolescent
migraine has become apparent whose significance,
however, is still uncertain.13
After all these years, the diagnosis is still
one of exclusion, being based upon excess crying
in the absence of a recognizable cause. This
puzzling lack of progress may suggest one of two
possibilities, either colic is such an
intractably difficult problem that 68 years was
simply too short an interval for a solution to
be found, or the research effort may have been
misdirected.
From a biological perspective, small infants are
primitive creatures who still function at a very
basic level of visceral brainstem reflexes,
because higher inhibitory modulating structures
are not sufficiently developed yet.14,15
This implies that any behavioral or
physiological dysregulation observed may
reasonably be expected to arise from this same
level. Yet, the possibility that infantile colic
could reflect a dysregulation at the brainstem
level has received scant attention.
In a recent study conducted in my clinic, a
5-point clinical index of vestibular
(hyper)activity was presented and applied as a
tool to evaluate brainstem dysregulation in
colicky babies before and after gentle treatment
compared to non-colicky babies (see information
box).11 Colicky babies, it appears,
are not just babies who cry a lot. They also
show clinical evidence of vestibular
dysregulation i.e., dysregulation at the
brainstem level. Before treatment, the
vestibular index was 7.8 times higher for
colicky than non-colicky babies. Following
treatment, the index had decreased by 96.5%,
signifying a normalization of vestibular
regulation.
In this review, relationships between infantile
colic and brainstem dysregulation are further
investigated, as is the role of upper-cervical
muscular dysfunction acquired at birth.
Colic and brainstem dysregulation
As one of the first sensory systems to emerge in
the embryological development of vertebrates,
the vestibular nuclei have extensive projections
to other brainstem nuclei and play a central
role in many regulatory processes.16,17
This means that any vestibular dysregulation
present may be propagated downstream to also
involve these other brainstem nuclei,
particularly those of the autonomic and the
trigeminal systems.18,19 Indeed, from
scattered sources throughout the literature,
supportive evidence of brainstem dysregulation
in infantile colic can be gleaned. Though little
studied, concomitant symptoms that are commonly
associated with colic include (1) asymmetric
posture (C-curve) and head preference even while
asleep, which may lead to developmental
plagio/brachiocephaly;20 (2) extensor
hypertonicity and pseudo-opisthotonic
posture;20,21 (3) upper-cervical
movement/joint dysfunction, muscular tightness
and occipital tenderness;20 (4) high
levels of stress and stress arousal;9,21,22
(5) (breast)feeding difficulties;23-26
(6) gastro-intestinal regulatory disorders such
as regurgitation /Ger(d) and intestinal
cramps.1
Extensor posture
Relaxed, happy babies have a snug,
flexion-dominated fetal posture.14
Their necks are wobbly and when held upright
against the parent’s chest the head needs to be
supported. In stark contrast colicky babies are
extension-dominated and arch their back.20
Parents must be alert not to let the baby slip
from their hands (back dive). These babies are
noted to have a “strong neck,” a “strong back”
and “strong legs” and, when held in front, they
try to climb up against the parent’s chest. When
placed in a prone position, they tend to lift
their head, pull up their legs and try to move
forward in a froglike fashion, even as early as
the first few days after birth. Because in young
infants, extensor posture and hypertonicity
point to activation of anti-gravity muscles by
the vestibulo-spinal tracts, the observed
postural characteristics (1,2,3) are suggestive
of vestibulo-spinal hyperactivity.15,16,27
Stress characteristics
Colicky babies are restless, irritable, in
obvious distress, have trouble falling asleep
and have fragmented sleep patterns (15-20 minute
cat naps), they scratch their face, are easily
startled, react strongly to minor sensory
stimuli (hyperreactivity, hyperarousal,
hypervigilance) and are easily
overstimulated.21 In addition, they
tend to have cold clammy hands and feet.
Together these symptoms point to sympathetic
activation, as do the shrill and high-pitched
acoustic characteristics of colicky crying.22,25,28-33
Studies of covariation of infant cry acoustics
and autonomic state have shown that the pitch of
infant cries and other aspects of vocal prosody
provide a sensitive index of autonomic
activity.34 Less vagal output is
associated with increased pitch, whereas
increased vagal output is accompanied by a
lowering of pitch. Shrill high frequency cries
indicate distress reflecting decreased vagal
output or increased sympathetic activation. In a
recent development a mobile telephone app
(“Chatterbaby”) incorporating a cry-translation
algorithm allowed discrimination of cries
associated with fussiness, hunger, pain and
colic with 70-90% accuracy.35 It was
found that the cries of colic were similar to
those of pain, but of higher intensity and
pitch, suggesting that colic may be painful and
stressful. Another study reported that increased
levels of salivary cortisol in colicky babies
were related to fragmented sleep patterns and
intensity of crying, suggesting activation of
the HPA-stress system.36 Actually,
the sympatico-adrenomedullary (SAM) and the
hypothalamic-pituitary-adrenocortical (HPA)
stress systems may both be activated.24
Feeding problems
Co-occurrences between infantile colic and
feeding problems are reported, but
interrelationships have been little studied. In
hospital-admitted colicky babies, feeding
problems were twice as common as in non-colicky
babies.24 In a different study
colicky babies had (i) more gastro-esophageal
reflux (GER); (ii) were less responsive during
feeding interaction with the mother; (iii) had
more episodes of feeding discomfort and (iv) had
greater difficulty coordinating sucking,
swallowing and breathing.23 This led
the authors to suggest that colic and feeding
problems could both be related to some
underlying disorder of behavioral dysregulation.
An association between feeding problems and
colic was also reported in a study that looked
at suck-swallow-breathing-coordination (SSBC) in
colicky and non-colicky babies.26 The
authors observed that the duration of feeding in
colicky babies was twice the normal 15-20
minutes in non-colicky babies. In addition,
colicky babies showed dysfunctional
relationships for elements of SSBC, similar to
but more subtle than those observed in infants
with neurological difficulties. Though in
colicky babies there is no evidence of
neurological deficit, the feeding difficulties
could still reflect a dysregulation of brainstem
autonomic nuclei, because sucking, swallowing,
breathing and vocalization are coordinated by
the nucleus ambiguus of the vagus system.28,37
Gastro-intestinal problems In
small infants, gastro-intestinal disorders
including regurgitation (gastro-esophageal
reflux, GER) constipation and intestinal cramps
with or without obstipation or dyschezia are
common in association with colic.1,38
Frequent associations are gas/bloating/colic,
gas/bloating/regurgitation and
regurgitation/colic. These symptoms have been
interpreted as early manifestations of later
childhood painful FGID’s.39-41
Regurgitation (Ger) involves a transient
relaxation of the lower esophageal sphincter
triggered by gastric stretch receptors and not
by passive mechanical distension of the
gastro-esophageal junction.42,43 This
may indicate that excessive regurgitation could
reflect dysregulation of autonomic neural
control. Alternatively, the infants could just
be nauseous due to dysregulation and
hyperactivity of the vestibular system.11,19
In case of constipation the presence of dry hard
stools may suggest decreased gut motility due to
decreased parasympathetic output or sympathetic
activation and point to autonomic
dysregulation.44 Infant dyschezia is
defined as excessive straining for more than
10-20 minutes with or without passing of stools1
and is thought to be due to failure to
coordinate intra-abdominal pressure with
relaxation of the muscles of the pelvic
floor.45 Again, this may point to
dysregulation of autonomic neural control.
Colic, upper-cervical dysfunction and mild
birth trauma
Scattered evidence suggests that the origin of
the upper-cervical muscular dysfunction and
occipital tenderness may be related to the
birthing process. One study documented an
association between colic and feeding problems
and found that the main risk factor was a
complicated pregnancy or birth process.24
Another study reported that breast feeding
problems were more common following assisted
births than non-assisted births.46
Stressed and difficult temperamental behavior
apparently are already present during the first
few days after birth,47 and high
responsivity (stressed) behavior during the
first week was predictive of colicky behavior
during the following weeks.48 A
recent MRI study revealed that already shortly
after birth “colicky babies showed greater
sensitivity to olfactory stimuli than their
non-colicky peers.”49
Biedermann20 was the first to have
specifically linked upper-cervical dysfunction
and colic to mild birth trauma related to the
difficult human birth process as compared to the
great apes. In the course of human evolution,
the development of bipedal locomotion and the
concomitant adaptation of the pelvic
architecture preceded the increase in brain size
by several million years.50 In modern
humans there is a very tight fit between the
size of the baby and the maternal birth canal
leaving only a small margin of error. As a
result, the human baby must negotiate a narrow
and tortuous birth canal51-53 leading
to a high level of birth complications with
mother and child in comparison to the great
apes.54 During birth the skull is
subjected to molding forces while the neck
undergoes a considerable degree of rotation and
extension.55,56 It is easy to
envisage how in a percentage of births such
twisting may result in upper-cervical movement
and joint dysfunction, muscular tightness and
tenderness,20 particularly in view of
the observation that small meningeal bleeds are
common even in non-symptomatic neonates.57,58
In most births the final exit turn is to the
right, and, accordingly, if there is a distinct
head preference, in 70-80% of cases this is also
to the right.59 In chimpanzees with
their easier birth process inconsolable crying
as in human colicky babies is unknown.60
Although infant chimps cry, they stop crying as
soon as they are handled by the mother.
Colic, brainstem dysregulation and
upper-cervical dysfunction
How these entities are interlinked may be
inferred from the realization that
upper-cervical proprioception plays an important
role in modulating the vestibular system, as
does the visual system.61-63 Afferent
proprioceptive input from upper-cervical
segments (C1-3) and from axial structures
project to the vestibular nuclei and indirectly
to the medial cerebellar cortex and its purkinje
cells and from there to the fastigial nucleus,
which is the output nucleus of the medial
cerebellum (Figure 1).16 By
inhibition of the fastigial nucleus the purkinje
cells of the medial cerebellum indirectly exert
an inhibitory modulating influence on the
vestibular system.16,19,27,64
Vestibular hyperactivity may arise even in case
of weak, subclinical, diminished cerebellar
inhibition.19,65 Consequently,
aberrant proprioceptive traffic into the
vestibular system and the medial cerebellum,
arising from tight sub-occipital musculature
acquired at birth could conceivably lead to
dysregulation and hyperactivity of the
vestibular nuclei. Conversely, treatment
achieving relaxation of the tight musculature
may be expected to restore regular
proprioceptive flow and facilitate normalization
of the inhibitory cerebellar modulation of the
vestibular nuclei.
Figure 1: Functional relationships of
sub-occipital musculature, medial cerebellar
nuclei, vestibular nuclei, reticular formation,
vagal nuclei and adrenals. PMRF – pontomedullary
reticular formation; NTS – nucleus tractus
solitarius; DM – dorsal motor nucleus;
NA-nucleus ambiguus; IML – intermediolateral
cell column.
Young infants in particular may be vulnerable to
vestibular dysregulation, because compensation
via the visual system would not be available as
visual gaze and the vestibulo-ocular reflex
(VOR) remain to be fully established.15
In small babies, vestibular modulation may be
almost entirely dependent on upper-cervical
proprioception. The vestibular and the fastigial
nuclei send efferent projections to the
autonomic nuclei and to the reticular formation,
and from the latter onwards to the sympathetic
chain and the adrenal glands (Figure 1).16,66,67
This means that dysregulation of the vestibular
nuclei may propagate along these projections to
also induce dysregulation of the sympathetic and
parasympathetic systems, such as inferred in the
above review of concomitant symptoms.
Colic and childhood/adolescent
migraine
Although a close association between colic and
migraine seems well established,13,68-70
the discussion of its significance is hampered
by the fact that there is no generally agreed
pathophysiological model for either of these
disorders. Some authors have suggested that
colic and migraine may share a common pathogenic
mechanism such as excessive sensitivity to
sensory stimuli71 or increased
sensitization of perivascular nerve endings in
the meninges and the gut,13 possibly
mediated by calcitonin-gene-related peptide
(CGRP). At least one case-control study found an
association between migraine and functional
gastro-intestinal disorders in children and
adolescents.72 Circadian rhythms have
also been suggested as being at the base of both
colic and migraine.71 Other authors
have suggested that there may be a continuum
from colic, as the earliest manifestation of
migraine, through other childhood precursors of
migraine, to migraine in adolescents and
adults.73
Discussion
It is proposed that in a percentage of births
the human baby may suffer mild trauma, as
initially suggested by Biedermann,20
and that this may have far reaching effects.11
The associated muscular tightness and
accompanying movement/joint dysfunction may have
an adverse effect on the vestibular and
autonomic systems of the brainstem. Via a
mechanism of aberrant proprioception, this may
lead to dysregulation/ hyperactivity of the
vestibular nuclei and the ensuing concomitant
autonomic symptoms of colic. Such a mechanism
may explain why in many babies the full spectrum
of colicky behavior is not reached until several
weeks after birth.9,10 The finding of
a 96.5% improvement of the vestibular index
following treatment consisting of mild sensory
stimulation11 is consistent with
restoration of regular proprioceptive flow and
normalization of vestibular modulation by the
medial cerebellum. It would suggest that central
neuromodulation may be accomplished not only by
cutaneous vibratory stimulation of the cymba of
the external ear (sensory neuromodulation),74
but also by similar proprioceptive stimulation
of the sub-occipital musculature, at least in
babies.11 The spontaneous resolution
of colicky behavior after 3-5 months may be a
consequence of developing cortical control and
inhibitory modulation of brainstem reflexes
during this same period and may, thus, represent
a developmental aspect of the disorder.15,37
However, this is not to say that in untreated
babies the underlying dysfunction also resolves
in all cases as there is accumulating evidence
of longtime sequelae.75,76 In a
10-year prospective study an association was
found between infantile colic and recurrent
abdominal pain, allergic disorders, sleep
disorders, fussiness, aggressiveness.77
A second study found that at three years of age
former colicky babies had more sleeping problems
and more frequent temper tantrums than former
non-colicky babies. Also, families with colicky
babies had more distress three years later.76
In a third study ex-colicky babies at four years
of age were more emotional and had more temper
tantrums and more complaints of stomachache.78
Infantile colic has also been linked to an
increased risk of Irritable-Bowel-Syndrome (IBS)
after four years of age.41 By
contrast, treated colicky babies three years
later were less likely to experience long-term
sequelae than colicky babies who had not been
treated.79
As to the nature of the link between infantile
colic and migraine, there is a tendency to not
only consider colic as the earliest age-specific
manifestation of migraine, but also implicitly
equate colic with early migraine.70,73
Some authors even went so far as to suggest that
migraine medication could be useful in
controlling colic.68 The
relationship, however, cannot be that
straightforward, because the great majority of
colicky babies do not develop migraine.
If colic is to be an early manifestation of
migraine, this would probably only apply to a
minority of genetically predisposed individuals.
In the only available cohort study, 23% of
ex-colicky babies developed migraine, 77% did
not and of the ex-non-colicky babies 11% still
did.80 From twin studies it is
estimated that 30-60% of migraine cases are
accounted for by genetics, which leaves a
remaining 70-40% to non-genetic external and
environmental factors.81 If, as
argued in this review, babies’ function at the
basic level of visceral reflexes and if
infantile colic is the clinical expression of
brainstem dysregulation, it would stand to
reason that the link with childhood migraine
should also be sought at this level.
Speculatively, and from an evolutionary
perspective, the high 15-25% prevalence of
infantile colic may be an inherent aspect of the
human condition and could be part of the price
we pay for our upright stance, bipedal gait, and
the difficult way we are born.
Future research
Given that after all those years the diagnosis
of infantile colic is still one of exclusion, it
is paramount that criteria be developed for a
diagnosis based on distinct and objective
clinical observations. A first step towards this
end has been made by the earlier study conducted
in my clinic in which a 5-point clinical index
of vestibular hyperactivity was presented and
applied to evaluate brainstem dysregulation in
colicky babies before and after treatment versus
non-colicky babies.11 This index
offers the prospect for development into a tool
for a positive diagnosis. The recognition of the
various concomitant symptoms reviewed above
allows additional clinical indices to be
developed i.e., postural index, stress index,
index of feeding behavior, regurgitation index,
index of gastric cramps. Once confirmed and
validated, these indices together with the
vestibular index may be integrated into a
comprehensive instrument toward an objective and
practical clinical diagnosis of infantile colic.
It is suggested that the focus of future
research should be broadened to also include the
associated symptoms that are indicative of
brainstem dysregulation. Also, the link with
childhood/adolescent migraine should be further
explored.
Conclusion
Colicky babies are much more than just infants
who cry a lot. They also show clinical evidence
of dysregulation at the brainstem level,
particularly of the vestibular and autonomic
nuclei. As a hypothesis it is proposed that
colicky behavior, vestibular dysregulation and
concomitant autonomic dysregulation are linked
to sub-occipital/ upper-cervical muscular
dysfunction secondary to mild birth trauma.
Treatment aimed at relaxing tight
sub-occipital/upper-cervical musculature
(sensory neuromodulation) may correct aberrant
proprioceptive outflow to the vestibular nuclei
and the medial cerebellum. This may facilitate
normalization of vestibular inhibitory
modulation by the cerebellum and lead to
improvement of brainstem regulation. It would
suggest that central neuromodulation can be
effectuated, not only by vibratory sensory
stimulation of the auricular branch of the vagus
nerve, but also by similar proprioceptive
stimulation of sub-occipital/upper-cervical
muscular structures, at least in babies.
Authors contribution
The author is solely responsible for all aspects
of this publication.
Funding
There was no external funding.
Competing interests
The author is director and owner of the clinic
Chiropractie Staphorst.
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