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Biological Basis ofPositional Head
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Deformations
ChristianLinz, FelixKunz, andTilmannSchweitzer
13
13.1 Growth Pattern
andPathogenesis
At birth, cranial sutures are physiologically not
fused [1], which allows for some movement
between the bony skull segments and enables a
certain degree of physiological reversible deformation of the skull, for example, when passing
through the birth canal [2]. This skull alteration
usually resolves itself within a few days [2, 3].
What is more, the patent sutures allow for expansion of the brain parenchyma, which leads to an
increase in volume of the skull, as reected in
its percentile growth [4]. The increase in brain
size serves as the critical force behind cranial
growth and causes the skull to nearly double in
size within the rst 6 months of life. The necessary intramembranous bone enlargement takes
place mainly by ossication at the bone margins
or at so-called osteogenic fronts of patent cranial
sutures. These sutures contain brous tissue and
C. Linz (*)
Department of Oral and Maxillofacial Surgery,
University Hospital of Würzburg, Würzburg, Germany
e-mail: linz_c@ukw.de
F. Kunz
Department of Orthodontics, University Hospital of
Würzburg, Würzburg, Germany
T. Schweitzer
Department of Neurosurgery, Section of Pediatric
Neurosurgery, University Hospital of Würzburg,
Würzburg, Germany
represent not only articulations but also the distinct sites at which osteogenesis takes place after
the proliferation and differentiation of osteoprogenitor cells [1].
The initially rapid growth rate of the brain
parenchyma then declines. After 2–4years, the
brain reaches 75% and after 6–8years 90% of its
nal volume, respectively, and reaches its nal
size at the age of 12. In the following years, the
bony skull continues to display a minor increase
in size, which is mainly due to a thickening of the
skull bones. However, almost all skull sutures
remain patent for some years thereafter: With the
exception of the metopic suture, which fuses by
the second year of life, other large sutures—such
as the sagittal, coronal, and lambdoid sutures—
do not fuse physiologically before the third
decade of life [1]. The fact that cranial sutures
remain patent is regulated by mechanical forces
as well as by factors that stimulate or inhibit bone
growth [5]. Different signaling pathways affect
the transcription factor RUNX2 [6], which is
decisive in regulating osteoblast activity [1].
This physiology of the cranial sutures results
in an easily moldable skull in the rst weeks and
months of life. During this period, external gravitational forces that act persistently on the same
region of the skull may cause a deformity of the
neuro- or viscerocranium. This is highly relevant since positioning of the baby—resulting in
corresponding external forces—represents such
a mechanism, which may then lead to an abnor-
© Springer Nature Switzerland AG 2021
U. Meyer (ed.), Fundamentals of Craniofacial Malformations,
https://doi.org/10.1007/978-3-030-46024-2_13
205
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C. Linz et al.
mal skull shape [7]. Supine positioning of the
baby—as recommended in order to reduce the
risk of sudden infant death syndrome—can thus
lead either to posterior attening of the entire
occiput (positional/deformational brachycephaly (DB)) or to one-sided occipital attening
(positional/deformational plagiocephaly (DP))
if the baby has a preferred side. As mentioned
above, both types of head deformities arise due
to lasting external molding forces, which alter
cranial growth and display criteria, which partly
overlap. However, a clear distinction between
DB and DP should be made [8].
13.2 Positional/Deformational
Brachycephaly (DB)
The prolonged inuence of an external force on the
entire occiput might cause DB, which is dened
as bilateral and therefore symmetric attening of
the occipital region, resulting in a reduced length
of the entire skull (Fig.13.1) [7, 8]. This reduction
in length leads to an increase of the cephalic index
(CI), which is dened by the ratio of the maximum
width to the maximum length of the head [10, 11].
While a brachycephalic head shape was dened by
a CI > 92–93% in earlier reports, recent publications dene a cut- off at a CI >94% [10, 12, 13].
This new cutoff point reects the general observation that the physiological width–length ratio of
infants’ skulls has changed in recent decades. While
a CI of 77% was considered normal in the 1970s,
recent publications report that a normal CI lies in
the range of 80–85% [9, 14–16]. Further possible
characteristics of brachycephaly include a compensatory widening of the occipital region [7, 17] and
of the fronto-lateral or temporo-occipital skull [17].
These changes lead to the characteristic appearance
of a trapezoidal head shape in vertex view.
In this context, it should be noted that purely
symmetric occipital attening occurs very rarely
since an asymmetric, unilateral occipital aspect is
very often detectable. As DB is dened as a symmetric deformity, a skull with such components
of asymmetry must be classied as representative
of a case of deformational/positional plagiocephaly (DP) [17].
13.3 Positional/Deformational
Plagiocephaly (DP)
The prolonged inuence of a unilateral external
force on the occiput might cause DP [18–20],
which is dened by a one-sided occipital attening of the head, resulting in an asymmetric
head shape (Fig.13.1). Currently, DP is dened
as a difference of more than or equal to 0.3cm
in both diagonal diameters of the head, measured on the horizontal plane [21]. In addition
to this unilateral decit, an ipsilateral anterior
shift of the ear and a compensatory bulging of
the ipsilateral forehead are further characteristics of DP [17, 22–25]. In some cases, facial
asymmetry is also possible, which often
involves an excess of fatty tissue and—in more
severe cases—some bony hyperplasia in the
area of the zygoma [17]. The extent to which
positional asymmetries affect the development
of mandible/maxilla, of dental occlusion, and
of potentially resulting malocclusions has not
been studied to a satisfactory degree; however,
several studies have indicated an association
between DP and lateral crossbites, particularly
on the contralateral side of the posterior skull
attening [26, 27].
While the above-mentioned CI is a suitable
parameter for describing the symmetric head
deformity found in DB, there are many ways to
classify the asymmetric head deformities caused
by DP, with cranial vault asymmetry (CVA) and
the cranial vault asymmetry index (CVAI) serving as the most common parameters [21, 28,
29]. As mentioned above, a brachycephalic
aspect exists in many DPs and goes hand in
hand with an altered CI; however, it is not used
for classifying DP as it does not take the asymmetric element into account. For detailed information on existing classications, see the
chapter “Diagnosis”.
13.4 Development ofDP/DB
Intrauterine restraints might lead to a skull deformity [30–32]. Childbirth is also associated with
several possible forces on the malleable skull as
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Positional deformational plagiocephaly
207
Typ 1:
Unilateral flattening
of occiput
Typ 4:
Facial asymmetry
Typ 2:
Forward shif
of the ear
Compensatory bitemporal prominence and
Positional deformational brachycephaly
Typ 3:
Forhead prominence
on the flattened occipital side
Typ 5:
vertical growth of occiput
Typ 1:
Flattening
of the entire occiput
Fig. 13.1 Positional plagiocephaly and brachycephaly as described by Argenta [7, 9]
Typ 2:
Widening
of the occiput
Compensatory bitemporal widening
Typ 3:
and vertical occipital growth
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C. Linz et al.
passage through the birth canal or the use of
obstetrical techniques (e.g., forceps, suction cup)
might cause skull deformations that are visible
directly after delivery [2, 32, 33]. Many of these
deformations resolve spontaneously and rapidly
within several days or weeks [2, 3, 34]. It is
important to differentiate these skull deformations from DP, the diagnosis of which should not
be determined before 6weeks of life. However,
birth deformations may persist and evolve into
DP [35], and some intrauterine and birth-related
conditions are thus also important risk factors for
developing DP (see also the Sect. 13.5 “Risk
Factors”).
The 1992 recommendation of putting infants
to sleep in the supine position (the so-called
“Back to Sleep” campaign) led to a drastic reduction of sudden infant death syndrome (SIDS), the
most common cause of infant mortality in industrialized nations [36, 37], and this reasonable recommendation should be therefore continued to
be followed [37, 38]. However, while the “Back
to Sleep” campaign has reduced the incidence of
SIDS by a power of ten, it has simultaneously led
to a roughly tenfold increase in DP [39].
While the incidence of isolated DB is low, DP
is the most common head deformity in otherwise
healthy infants. The incidence of DP reported in
the literature ranges from around 0.3% up to
50%, a very wide range that can be explained by
varying cohorts, differing time points of investigation, and varying classications [8, 40–42].
According to Ahluwalia etal., nearly one in four
children is affected by some degree of deformational skull abnormalities [43]. The incidence of
DP is age dependent, with a peak of prevalence
within the rst 6months of life. Increasing incidence can be observed between the sixth week
and the fourth month of life [40, 44]. In the following months and up to the 24th month of life,
the incidence decreases to 3.3% [3, 44]. However,
one prospective epidemiologic study described
moderate to severe asymmetries in 1% of investigated children of age 5.5years [40]. A study on
adolescents (ages 14–17years), all born after the
recommendation to place babies on their back
had been made (“Back to Sleep” campaign,
1992), described a persisting skull deformity in
2.1% of the cohort [45]. In addition to the aforementioned differences in the incidence of positional deformities, the described rate of
spontaneous improvement varies among studies
[27, 44, 46]. This nding may again be explained
by differences in age, data collection, and methods among studies, which would also explain
why a few studies assume improvement without
treatment, whereas most existing studies recommend stage-related therapy [47, 48].
13.5 Risk Factors
A variety of risk factors are involved in the pathogenesis of positional head deformities, though
there is poor concordance regarding clear risk
factors in the literature [49]. To provide a better
understanding of the risk factors, we subdivide
prepartum, peripartum, and postpartum factors.
13.5.1 Prepartum Factors (Including
Preexisting Determinants)
The incidence of DP/DB nearly doubles in male
babies, who are usually bigger than girl babies
[3, 18, 31, 32, 42]. This increased incidence
becomes relevant due to the consecutively
reduced intrauterine space [8, 31]. The same
condition is apparent in multiple births and is
reported as a further risk factor [50, 51]. In the
same context, forced abnormal intrauterine
positions are also mentioned as predisposing
factors [3, 50, 52, 53]. Positional head deformities are also more common in children of primiparae [44, 50, 54]. A younger age of the
mother and a lower educational status have been
reported as potential sociodemographic risk factors [44, 50, 54–57].
13.5.2 Peripartum Factors
Known risk factors for the development of an
abnormal skull shape include younger gestational
age, the associated decreased mobility of the preterm baby, and the resulting earlier exposure of
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209
the very malleable skull to external positional
forces [5, 50, 52, 55, 57].
Furthermore, a higher birth weight and large
head circumference also lead to an increased rate
of a deformed head shape [3, 7, 52, 58, 59]. These
abnormal head shapes can also result from
difcult deliveries and the usage of a ventouse
cup or forceps [44, 50, 53, 54].
13.5.3 Postpartum Factors
A positional preference for one side represents an
important risk factor [5, 14, 50–52, 54–57, 59].
In this context, mobility restrictions of the cervical spine—caused, for example, by bleeding into
the sternocleidomastoid muscle or by torticollis—are predisposing conditions for developing
DP [3, 14, 35, 50, 52, 58, 60]. While torticollis is
present in only 0.1–2% of children with a symmetrical head shape, its incidence increases to up
to 20% in children with DP [3]. At least 8% of
children younger than 16weeks have a preferred
sleeping side, often the cause of a developing
DP.One contributing factor to DP is formed by
unilateral stimuli, such as a baby’s unchanged
feeding position [46, 56, 57, 59]. Bottle-feeding
without changing position is therefore associated
with an increased risk of DP in contrast to breastfeeding with a changing position, which has a
protective effect [18, 46]. Another protective
effect is achieved by the so-called tummy time—
that is, putting the baby in the prone position
while awake and under observation [61, 62].
The supine position—which is recommended
in the valuable guideline that prevents SIDS—is
also one of the main risk factors discussed in
developing positional head deformities [7, 14,
32, 42, 44, 50, 51, 63]. The use of car seats,
swings, carriers, bouncy seats, and rockers is
associated with an increased risk of skull deformities, as is parents’ smoking [7, 54].
Every developmental delay that is accompanied by reduced activity also correlates with an
increased risk of deformational skull deformity
[50, 52, 54, 59].
Ultimately, the pathogenesis, the underlying
mechanisms of skull deformation, as well as
disease- promoting factors and their inuence
have not yet been fully explained [8, 18].
13.6 Impairment
ofNeurocognitive
Development
Several reports on developmental delays in the
context of deformational skull abnormalities
exist [64–66]. However, comparing of infants
with and without skull deformity, it should be
noted that most children score within the average
range of the test norms [67].
A few reports of differences in motor development have been reported for infants within the
rst months of life exist. However these differences between affected and non- affected infants
decrease at the age of 3, when differences in cognition and language become apparent. Infants
with mild DP/DB display minimal—if any—differences, whereas infants with more severe forms
demonstrate statistically signicant differences.
These motor developmental delays can also be
reected in deferred vocal and language development since speech is based on a ne coordination
between laryngeal and supra-laryngeal mechanisms, including auditory feedback. These mechanisms require very rapid neuro-physiological
control, which leaves no time for compensatory
regulation in the case of dysfunction. However, in
examinations, it has not yet been possible to demonstrate an association between delays in early prespeech babbling articulatory skills or early
language production on the one hand and positional skull deformities on the other hand [68–70].
However, a signicant relationship between
preterm birth on the one hand and neonatal complications, mortality, and developmental delay on
the other hand is known to exist [71].
Consequently, a preexisting developmental delay
is a possible reason for deferred mobilization
causing extended time for the inuence of external forces on the infant’s skull. This fact highlights the difculty of differentiating between
cause and consequence in the question of a possible association between developmental delays
and deformational head abnormalities.
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In general, it should be noted that many studies exhibit methodological problems, such as the
use of non-homogenous groups, a lack of
standardized testing or of control groups, or the
insufcient consideration of inuencing variables, such as socioeconomic status, the parents’
IQ, or individual support.
We regard a developmental delay as a risk factor for positional skull deformations [72]. The
fact that slight decits might either precede or
follow DP/DB highlights the need for close monitoring of affected infants since an association of
any kind with a developmental risk is possible.
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