Continuing Education Activity

Plagiocephaly refers to an oblique or asymmetrically shaped head caused by unilateral flattening, arising either from premature fusion of a cranial suture or from external deformational forces. Synostotic plagiocephaly results from early coronal or lambdoid suture closure and leads to characteristic skull and facial asymmetries, potential increases in intracranial pressure, and risks of visual impairment. Deformational, or positional, plagiocephaly develops from intrauterine constraint or sustained postnatal positioning and remains far more common. This course reviews the accurate differentiation of plagiocephaly that relies on physical examination, anthropometric measurements, and imaging to confirm suture patency and assess severity.

This activity discusses the etiologies, distinguishing features, diagnostic strategies, and management options for both synostotic and deformational plagiocephaly. Participants will gain an in-depth understanding of the early clinical signs, interpretation of imaging findings, and evidence-informed conservative or surgical interventions. This activity for healthcare professionals is designed to enhance the learner's competence in identifying plagiocephaly, performing the recommended evaluation, guiding families on repositioning, tummy time, helmet therapy, and referral pathways, and implementing an appropriate interprofessional approach when managing this condition to enhance early identification, optimize developmental outcomes, and support coordinated, patient-centered care.

Objectives:

• Identify clinical features that distinguish the various types of plagiocephaly.
• Apply evidence-based conservative management strategies for plagiocephaly.
• Determine indications for timely surgical intervention for plagiocephaly surgery.
• Apply interprofessional team strategies to improve care coordination and outcomes in patients with plagiocephaly.

Introduction

Plagiocephaly denotes an oblique head shape.[1] The Greek terms plagios and kephale translate to oblique and head, respectively. Plagiocephaly reflects an asymmetric head contour produced by unilateral flattening, and the term flathead functions as a synonymous description. Clinicians classify plagiocephaly as synostotic or deformational.[2]

The International Classification of Diseases defines isolated synostotic plagiocephaly as a nonsyndromic craniosynostosis pattern characterized by premature fusion of 1 coronal or lambdoid suture, leading to skull deformity and facial asymmetry. Unilateral coronal synostosis produces anterior plagiocephaly, while premature fusion of the lambdoid suture produces synostotic posterior plagiocephaly.[3] Deformational plagiocephaly results from intrauterine or postnatal external forces that modify skull shape, and many sources refer to this condition as positional plagiocephaly.[4][5][6][7][8][4] Positional plagiocephaly describes deformation of a normal, compliant skull caused by external pressure in the absence of synostosis.

Etiology

More than 95% of cases of nonsyndromic craniosynostosis occur sporadically.[9] Positive family history is present in 8% to 15% of patients with nonsyndromic coronal synostosis, whereas lambdoid synostosis shows a 0% to 6% familial incidence.[10] Coronal suture closure begins at approximately 24 years of age, and lambdoid closure begins at 26 years of age. Craniosynostosis involves premature suture fusion that forms osseous bridging and typically produces an abnormal head shape.

Intrauterine deformational forces include an abnormal fetal position, irregular uterine shape, compression of the fetal head during descent into the pelvis, or mechanical effects from multiple gestation. Postnatal deformational forces most often result from prolonged head positioning. Craniosynostosis results from multifactorial influences, including intrinsic bone abnormalities, genetic mutations, and environmental factors.[11][12] Associations include hypophosphatemia, rickets, hyperthyroidism, preterm delivery, low birth weight, teratogenic exposures, valproic acid, and shunted hydrocephalus. Mouse studies demonstrate that fetal head constraint triggers upregulation of TGF-beta receptor 1 and 2 and FGFR2 at the coronal suture, promoting coronal synostosis.[13] Mutations involving TWIST, FGFR2, and FGFR3 contribute to unilateral coronal synostosis.[14]

Incidence of deformational plagiocephaly rose after the 1992 “Back to Sleep” campaign, which encouraged a supine sleep position and simultaneously reduced sudden infant death syndrome.[15][16] Risk factors include abnormal intrauterine presentation, forceps or vacuum-assisted delivery, first-born status, prematurity, multiple gestation, male sex, larger head circumference, supine sleep position, limited neck rotation, congenital muscular torticollis, low activity, insufficient tummy time, and neonatal brachial plexus palsy.[15][6][17][8][18] Tummy time refers to awake, prone positioning. Congenital muscular torticollis often leads to a persistent head preference that exerts prolonged pressure on one side, resulting in unilateral flattening.[18]

Epidemiology

Anterior plagiocephaly occurs in approximately 1 in 10,000 live births and accounts for 13% to 16% of craniosynostosis cases.[19] Unilateral coronal craniosynostosis develops 4 to 7 times more frequently than bilateral coronal synostosis, with a male-to-female ratio of 1:2. Unilateral lambdoid synostosis represents 1% to 5% of craniosynostosis, with an approximate occurrence of 1 in 33,000 births.[20][21]

Deformational plagiocephaly affects 15% to 20% of infants, although some reports note an incidence as high as 46.6%.[22] Prevalence trends are slightly higher in males, at 1 to 3:1, and they typically receive a diagnosis before 4 months of age. Before 1992, deformational plagiocephaly appeared in roughly 1 in 300 infants, but the “Back to Sleep,” now “Safe to Sleep,” campaign produced a 400% to 600% increase.[21][23][24][25]

Secondary craniosynostosis develops in systemic disorders (eg, rickets and hypothyroidism) in newborns with microcephaly and after shunt placement for hydrocephalus.[26]

Pathophysiology

Positional plagiocephaly typically results from mechanical forces on the head in 1 position, often due to habit, intrauterine pressure, or torticollis. The skull flattens due to a more frequently focused gravitational force on the same area, increasing the flattening effect (see Image. Positional Plagiocephaly).[18] Premature sutural fusion in craniosynostosis can result in elevated intracranial pressure (ICP), which can lead to cognitive impairment.[12] Elevated ICP is associated with poorer performance on psychometric testing.[18]

History and Physical

In synostotic anterior plagiocephaly, the forehead appears flattened, and the supraorbital margin sits high.[26] The opposite side of the forehead pushes forward, and the nasal septum may deviate toward the normal side. Strabismus develops in 50% to 60% of patients because dysfunction of the superior oblique muscle follows alterations in the orbital roof and trochlea.[27] Mandibular deviation and occlusal changes may also occur, and a palpable bony ridge often follows the fused suture. Synostotic posterior plagiocephaly produces frontal and occipital bossing on the opposite side, along with downward displacement of the ipsilateral ear and mastoid.[26] From an overhead view, the skull adopts a trapezoid configuration.

Distinguishing deformational from synostotic posterior plagiocephaly can be challenging, although deformational plagiocephaly is more common.[21] Several features help separate deformational plagiocephaly from lambdoid synostosis (see Image. Plagiocephaly Types).[27] Lambdoid synostosis presents at birth, while deformational plagiocephaly typically emerges weeks later. A preferred sleeping position often appears in the history of deformational cases. A bony ridge along the suture and a bulging mastoid accompany lambdoid synostosis. Frontal bossing appears ipsilateral in deformational plagiocephaly and contralateral in lambdoid synostosis. Contralateral occipital bossing characterizes deformational plagiocephaly. Ipsilateral ear displacement shifts anteriorly in deformational plagiocephaly and posteriorly in synostosis, although some authors question the reliability of ear position.[21][28] The skull resembles a parallelogram in deformational plagiocephaly and a trapezoid in lambdoid synostosis (see Image. Plagiocephaly).

Features of increased ICP may be present in 15% to 20% of children with coronal or lambdoid synostosis, yet symptoms, eg, headache, vomiting, altered sensorium, and bulging fontanelle, often remain absent.[29] Papilledema provides the most reliable indicator of ICP in craniosynostosis, with a specificity of 98%.[30] Chronic ICP elevation can culminate in optic atrophy, leading to blindness and subnormal intelligence.[29]

Evaluation

Computed tomographic (CT) scanning with 3-dimensional (3D) reconstruction functions as the principal imaging modality for evaluating craniosynostosis.[21][31][32] A 64-slice multidetector CT scan evaluates the vault and skull base with reasonably low radiation exposure.[33] Premature fusion of a suture restricts growth perpendicular to the affected suture, with compensatory overgrowth along the remaining patent sutures.[34] CT findings of a prematurely fused suture include perisutural sclerosis, bony bridging, or complete loss of the suture. CT also supports quantitative assessment of the anterior cranial fossa, orbit, and ear in anterior synostotic plagiocephaly.[35] In deformational plagiocephaly, CT demonstrates a patent lambdoid suture and ipsilateral frontal bossing, in contrast to lambdoid synostosis. No significant distortion of the anteroposterior skull base axis appears in deformational plagiocephaly, and the chondrocranium maintains symmetry.[36] The cranial vault asymmetry index quantifies the severity of positional plagiocephaly.[18] The formula uses 100 multiplied by the difference between cranial diagonal diameters divided by the shorter cranial diagonal diameter. Values greater than 3.5 indicate severe asymmetry.

Unilateral coronal synostosis produces a shallow ipsilateral anterior cranial fossa, contralateral frontal bossing, and elevation of the roof and lateral orbital wall on the affected side, creating the characteristic “harlequin eye” sign. Unilateral lambdoid synostosis produces ipsilateral occipitoparietal flattening, contralateral frontal and occipitoparietal bossing, a small unilateral posterior cranium, and a tilted skull base. An ipsilateral deviation of the posterior fossa appears on endocranial skull base views in unilateral lambdoid synostosis. Morphometric skull base analysis using 3D CT differentiates the 3 causes of plagiocephaly.[37] Skull base asymmetry localizes to the anterior and middle cranial fossae in coronal synostosis and to the posterior and middle cranial fossae in lambdoid synostosis.

Lambdoid synostosis can crowd the posterior fossa and promote herniation of the caudal cerebellum through the foramen magnum, resulting in Chiari malformation.[29] Hydrocephalus and syringomyelia may also occur and are better visualized with brain magnetic resonance imaging (MRI). Conventional MRI does not adequately delineate sutures. A gradient-echo sequence known as “Black Bone” MRI displays a patent suture as a hyperintense signal, with loss of that signal when the suture has closed.[38]

Anthropometric measurements obtained with calipers aid in grading the severity of plagiocephaly.[23] Deformational plagiocephaly produces a measurable difference between diagonal occipital-frontal transcranial diameters, known as the transdiagonal difference, which quantifies asymmetry. Severity can also be graded by the difference between diagonal lengths on each side of the head.[18] A difference of 9 to 12 mm reflects mild to moderate asymmetry, and values greater than 12 mm reflect severe asymmetry. The cranial vault asymmetry index, calculated as 100 times the difference between cranial diagonal diameters divided by the shorter cranial diagonal diameter, identifies severe asymmetry when greater than 3.5.

Treatment / Management

Conservative Management

Conservative treatment serves as the first-line approach for patients with deformational plagiocephaly and mild unilateral synostosis.[26] Careful evaluation through physical examination and diagnostic imaging must rule out synostosis before adopting a conservative strategy for posterior plagiocephaly.[39] Management of deformational plagiocephaly focuses on sleep posture modification, counterpositioning, toy-assisted mobilization to stimulate the infant, physiotherapy for torticollis, supervised tummy time, and helmet therapy.[1][4][40][7]

Helmets become necessary when infants do not demonstrate improvement with repositioning techniques. Helmet therapy, introduced in 1979 by Clarren et al using a fiberglass model, functions as a molding device and currently involves custom fabrication for each child.[5][41] Customized helmets consist of high-density, hypoallergenic medical-grade foam.[18] A 3D laser scan of the infant’s head guides helmet creation, allowing a tight fit around protruding areas while providing space over flattened regions (see Image. Postcraniotomy Image). This design limits the growth of prominent areas and permits the expansion of flattened regions.

Optimal helmet therapy occurs at 5 to 6 months of age and loses efficacy after 18 months.[4] Adverse effects may include contact dermatitis and pressure sores.[5] Despite limited Class I evidence, meta-analyses demonstrate helmet therapy significantly improves cranial positional deformities.[42] The Congress of Neurological Surgeons recommends helmet therapy during the appropriate infancy period for severe deformities.[43]

Surgical Management

Surgical intervention becomes necessary in nonsyndromic craniosynostosis to correct morphologic abnormalities, prevent increased intracranial pressure, and mitigate psychosocial consequences. Surgical goals focus on achieving adequate intracranial volume for brain growth and restoring skull shape.[20] Procedures involve the removal of the fused suture and remodeling of both hypoplastic and compensatory growth regions.[4] Optimal timing for surgery falls between 6 and 12 months, coinciding with the most active phase of brain and cranial development.

Surgical options include open craniotomy with reconstruction or endoscopic suturectomy. Techniques vary from fronto-orbital remodeling for anterior plagiocephaly to occipital advancement for posterior plagiocephaly.[44] Additional methods include open calvarial reconstruction, strip craniectomy with implantation, barrel stave osteotomy, endoscopic suture release, and cranial distraction osteogenesis.[11][21][45] In open procedures, surgeons identify the fused suture, remove the bone flap containing the suture, remodel it, and achieve fixation with resorbable plates (see Image. Intraoperative Cranial Anatomy).[26] Cranial distraction osteogenesis employs distractors at osteotomized sites, with slow, incremental expansion over several weeks.[45] Some patients present with refractory torticollis accompanying synostotic posterior plagiocephaly, which may require sternocleidomastoid release.[21][31] Surgical correction successfully resolves preoperative papilledema in approximately two-thirds of patients with posterior synostotic plagiocephaly.[32]

Cranial bones retain flexibility until 6 months, allowing manipulation through endoscopic approaches.[26] Open surgery becomes preferable after this age. Endoscopic surgery offers shorter operative times, reduced blood loss, and faster recovery, and endoscopically assisted minimally invasive procedures have gained wider adoption.[46] Postoperative helmet therapy remains essential after endoscopic procedures. Children with unilateral coronal synostosis who undergo endoscopic strip craniectomy and helmet therapy demonstrate improved ophthalmic outcomes, including reduced amblyopia, astigmatism, and strabismus.[47]

Differential Diagnosis

The principal differential diagnosis in plagiocephaly involves distinguishing deformational (positional) plagiocephaly from synostotic plagiocephaly caused by premature suture closure. Anterior plagiocephaly typically results from coronal synostosis, while posterior plagiocephaly requires careful differentiation between synostotic and deformational types. Posterior synostotic plagiocephaly often receives misdiagnosis as positional plagiocephaly.[32]

Key historical factors include presence at birth, preferred sleep position, and improvement over time.[27] Craniosynostosis presents congenitally, whereas deformational plagiocephaly typically develops during the neonatal period. A history of a preferred sleep position frequently appears in deformational plagiocephaly, and positional deformities tend to improve as the child gains head control. In contrast, deformities caused by synostosis worsen over time.

Unilateral lambdoid synostosis produces a thick ridge along the fused suture with compensatory contralateral parietal and frontal bossing.[48] Ipsilateral occipitomastoid bulging and posteroinferior displacement of the ipsilateral ear characterize this condition, which contrasts with deformational plagiocephaly. Overhead observation reveals a trapezoid head shape in lambdoid synostosis and a parallelogram in deformational plagiocephaly. Diagnosis is confirmed by 3D CT imaging. Torticollis commonly accompanies deformational plagiocephaly, while Chiari malformation may occur in cases of lambdoid synostosis.

Prognosis

In deformational plagiocephaly, early initiation of conservative treatments yields satisfactory outcomes.[18] The high plasticity of the infant skull supports effective correction during early infancy. Physiotherapy plays a key role in improving congenital muscular torticollis, which often accompanies positional deformities.

Evidence indicates that nonsyndromic single-suture synostosis may cause persistent neuropsychological deficits. Surgical intervention enhances motor and cognitive function, particularly in severe craniosynostosis. Long-term follow-up after surgery frequently demonstrates normal academic performance and social function.[32] Untreated or uncontrolled craniosynostosis can result in increased intracranial pressure and cognitive impairment.[29] Surgical correction of synostotic plagiocephaly achieves significant improvement in cranial shape and yields high levels of parental satisfaction.

Complications

Plagiocephaly Complications

Deformational plagiocephaly usually corrects with frequent repositioning of the baby; however, it can produce cosmetic deformities if not treated adequately. Positional plagiocephaly can lead to developmental delay, musculoskeletal problems, and facial deformities.[7][49] Untreated unilateral coronal plagiocephaly may cause strabismus, astigmatism, amblyopia, and mandible malalignment.[47] Posterior synostotic plagiocephaly can lead to ophthalmologic, cognitive, and aesthetic sequelae.[32]

Surgical Complications

Surgical complications after synostotic plagiocephaly correction are usually relatively few and minor and do not produce permanent sequela.[21][32] The following complications are associated with the surgical treatment of isolated and syndromic craniosynostosis: 

• Excessive blood loss
• Venous air embolism
• Consumption coagulopathy
• Cerebrospinal fluid leak
• Dural tears
• Hyperthermia
• Hypoactivity
• Wound infection local
• Epidural abscess
• Ear infections
• Subcutaneous hematoma
• Epidural hematoma
• Residual plagiocephaly
• Reoperation [26][44][45][50]

Those patients with craniofacial syndromes are more prone to surgical complications. Blood transfusion requirements are reduced with endoscopic procedures compared to open procedures.[46]

Helmet Therapy Complications

Helmet therapy can lead to rare complications, including:

• Inadequate correction 
• Pressure damage to the skin at the site of application 
• Scalp erosion, ulcer, and temporary hair loss
• Contact allergic dermatitis [18]

Postoperative and Rehabilitation Care

Postoperative monitoring of the child should occur in the pediatric intensive care unit, particularly following open surgery.[50] Close observation of volume status, hemoglobin, hematocrit, and cardiovascular function is essential. Paracetamol provides effective pain relief, while sedatives should be avoided in extubated children. Invasive monitoring may be discontinued the following day if the child remains stable.

Deterrence and Patient Education

Early diagnosis and appropriate treatment of synostotic plagiocephaly can prevent aesthetic sequelae in children. Deformational plagiocephaly treatment primarily includes position behavior modification; however, in some cases, additional measures are necessary, including helmet therapy.[39] 

Parents should be educated about positioning and the use of tummy time. Intervention should be started as soon as the diagnosis is made. Deformational plagiocephaly does not result in developmental or neurocognitive delays.[32]

Enhancing Healthcare Team Outcomes

Plagiocephaly, defined as an asymmetric head shape caused by unilateral flattening, encompasses deformational and synostotic types. Deformational plagiocephaly often results from positional forces in utero or postnatally, whereas synostotic plagiocephaly arises from premature suture closure and requires surgical intervention. Early recognition and accurate diagnosis are essential, as differentiating lambdoid synostotic plagiocephaly from deformational plagiocephaly determines the appropriate management pathway. Conservative measures such as positional modification, supervised tummy time, and, in selected cases, helmet therapy, can effectively treat deformational plagiocephaly, while surgical correction addresses synostotic deformities to prevent aesthetic, neurological, and intracranial complications. Parental education on positioning, tummy time, and early intervention forms a critical component of care.

Effective management relies on interprofessional collaboration. Physicians, advanced practitioners, and general practitioners assess and diagnose cranial deformities and coordinate surgical or conservative management. Nurses monitor vital signs, administer medications, evaluate scalp dressings, and provide family education. Pharmacists ensure appropriate analgesics, antiemetics, and antibiotic regimens for postoperative care. Complex syndromic cases require coordinated care among pediatric neurosurgeons, plastic surgeons, and maxillofacial surgeons. Open communication, shared decision-making, and team-based strategies enhance patient-centered care, improve outcomes, safeguard patient safety, and strengthen team performance.

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Disclosure: Ajaya Kumar Unnithan declares no relevant financial relationships with ineligible companies.

Disclosure: Reddog Sina declares no relevant financial relationships with ineligible companies.