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Facial Asymmetry: A Narrative Review of the Most Common Neurological Causes

Justyna Chojdak-Łukasiewicz
* and
Bogusław Paradowski
Department of Neurology, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland
Author to whom correspondence should be addressed.
Symmetry 2022, 14(4), 737;
Submission received: 29 January 2022 / Revised: 30 March 2022 / Accepted: 2 April 2022 / Published: 4 April 2022
(This article belongs to the Special Issue Dentofacial Asymmetry — Challenges and Perspectives)


Symmetry of the face is one of the most important features for the perception of attractiveness. Asymmetry of the face means that the right and left sides of the face are not identical. Subclinical facial asymmetry is very common in the general population. Most people have some slight facial asymmetry, and this is the normal biological situation in humans. Abnormalities from soft tissue, dental, and skeletal elements lead to facial asymmetry. Asymmetry has many causal factors, and its aetiology includes both congenital and acquired conditions. Neurological facial asymmetry is scarcely addressed in the dental literature. In this narrative review, we focus on the most common neurological causes of facial asymmetry. From a neurological point of view, facial asymmetry can result from disturbances of the cranial nerves, developmental disorders, or myopathies. In the broad range of differential diagnostics of facial asymmetry, neurological abnormalities should be taken into consideration. The treatment must be related to the underlying cause. Complete knowledge of the aetiological factors and the character of the asymmetry plays a crucial role in formulating a treatment plan.

1. Introduction

Symmetry of the face is the one of the most important features for the perception of attractiveness. The word “symmetry” derives from Greek and comes from “syn” (together) and “metron” (meter). Symmetry means that both sides of the face, right and left, are alike. The term “asymmetry” refers to dissimilarity between components, altering the balance between structures. When applied to facial morphology, symmetry refers to the correspondence in the size, shape, and arrangement of facial features on opposite sides of the median sagittal plane [1]. Soft tissues, bones, and teeth contribute to symmetry. Asymmetry denotes disturbances between these components [2,3]. Most people have some slight facial asymmetry, and this is the normal biological situation in humans; i.e., the two sides are not perfect mirror images [4]. When photographs of the face are compared with photographs consisting of two left or two right sides of the face, we observe three different faces. This is called natural subclinical asymmetry and is a normal situation. The degree of asymmetry has a negative impact on functional and facial aesthetics. Anthropological research has shown that symmetry and averageness are important keys to the attractiveness of human faces [5,6].
The concept of facial symmetry is very significant to attractiveness. The problem of facial asymmetry is complex and has a wide range of possible causes. Analysis of facial features is useful for dentists, surgeons, orthodontists, and aesthetic medicine specialists. The causes of facial asymmetry are significant, especially from the orthodontic and dental points of view.
In this narrative review, we concentrate on the most important neurological causes of facial asymmetry.

2. Methods

To prepare this manuscript, PubMed and Google Scholar search engine results from the last 10 years were used. The search was conducted using three keywords: ‘facial’ or ‘face’ and ‘asymmetry’. The most relevant papers were screened by both authors. The references from qualifying publications were searched online for their relevance to the topic. Studies published in the English language were considered. Thirty-one publications were found to be the most relevant to the study and included in this review at the end of the selection process. We decided to proceed with a narrative rather than systematic review due to the characteristics of the articles found. A simple chart of the selected publications is presented in Figure 1.

3. Results

The neurological causes of asymmetry of the face can be divided into four groups: anomalies of the cranial nerves, developmental disturbances, myopathies, and other causes, such as headaches (Table 1). Cranial nerve damage, especially the affection of oculomotor, trochlear, trigeminal, and facial nerves, may occur in many neurological conditions. The most common acquired causes of cranial nerve damage are cerebrovascular events, such as ischemic or haemorrhagic stroke. Developmental disorders include several disorders that interrupt normal growth in childhood. Another cause of facial asymmetry is a group of myopathies.

3.1. Cranial Nerves

3.1.1. Nerve III (Oculomotor Nerve)

The third cranial nerve is a mixed nerve and provides motor, parasympathetic, and sympathetic fibres. The oculomotor nerve innervates the extraocular muscles (levator palpebrae superioris, superior rectus, inferior rectus, medial rectus, and inferior oblique), which are responsible for eyeball and upper eyelid movements [7]. Injury to the oculomotor nerve is characterised by ptosis (a drooping upper eyelid) secondary to paralysis of the levator palpabrae superioris and unopposed activity of the orbicularis oculi muscle [8]. Ptosis leads to a characteristic “sleepy” appearance and asymmetry in both unilateral and bilateral cases. The most common causes of third nerve palsy are presumed to be microvascular trauma and compression resulting from a neoplasm or an aneurysm [9,10,11].

3.1.2. Nerve IV (Trochlear Nerve)

The trochlear nerve is a motor nerve responsible, together with the oculomotor nerve and the abducens nerve, for eye movement. It is the smallest of the cranial nerves and has the longest course. The trochlear nerve innervates the superior oblique muscle and controls the abduction and intorsion of the eye [12]. Palsy of the trochlear nerve is characterised by vertical diplopia exacerbated when looking downwards and inwards. A patient can also develop compensatory head positioning, tilting away from the affected side. The three most common causes of trochlear palsy are trauma (especially to the occiput), ischemic or vascular damage (microvascular lesions associated with hypertension, diabetes mellitus, or vasculitis), and congenital disorders [13].
Congenital trochlear palsy typically presents with a long-standing compensatory head tilt and facial asymmetry from the head tilt. Congenital superior oblique palsy (SOP) is one of the most common causes of ocular torticollis in children, leading to asymmetric development of the face [14]. Congenital palsy of the trochlear nerve may be sporadic or genetic. This familiar condition is a rare, autosomal-dominant inherited disease characterised by congenital fourth cranial nerve palsy, facial asymmetry, and superior oblique tendon abnormalities (absence, redundance, misdirection) [15]. Children with torticollis tilt their heads to use both eyes together, a strategy that is associated with progressive facial asymmetry. The symptoms of superior oblique palsy are hypertropia in the affected eye, an abnormal head position, and excyclotorsion [16]. Deviation of the nose and mouth toward the hypoplastic side can be observed.

3.1.3. Nerve V (Trigeminal Nerve)

The trigeminal nerve is a mixed nerve and consists of a sensory and a motor part. The three sensory branches innervate the face, mucous membranes, and sinuses. The third branch (mandibular) of the trigeminal nerves has motor fibres. It innervates the muscles of mastication (medial pterygoid, lateral pterygoid, masseter, and temporalis) and the anterior belly of the digastric, mylohyoid, tensor veli palatini, and tensor tympani. Pure unilateral trigeminal motor neuropathy (UTMN) is a rare condition resulting from paralysis of the motor branch of the trigeminal nerve without sensory disturbances or lesion of other cranial nerves [17]. The first description was published in 1988 by Chia et al. [18]. The most common postulated aetiological factors of UTMN include viral infection, tumours, head trauma (skull base fracture of the oval foramen or pontine haemorrhage), autoimmune-inflammatory causes (e.g., Sjögren’s syndrome), and factors of vascular origin. In some cases, the condition is idiopathic [17,19,20,21]. A common clinical presentation is unilateral asymmetry of the face preceded by a feeling of wasting and weakness of the masticatory muscles. In addition, chewing problems and deviation of the jaw can be observed. The typical finding from magnetic resonance imaging (MRI) of the brain is replacement of the muscle by fat tissue [22].

3.1.4. Nerve VII (Facial Nerve)

The facial nerve is a mixed nerve containing both motor and sensory components [23]. The nerves emerge from the pons and carry motor fibres, which control all the muscles of the face. Anatomically, the upper part of the face (the eyes and forehead) is innervated from both hemispheres, while the lower part of the face receives innervations from the contralateral hemisphere [24]. Symptoms of facial nerve palsy depend on the location of injury. Supranuclear lesions affect upper motor neurons and manifest as central facial nerve palsy. Intranuclear locations of lesions, distal to the facial nerve nucleus, display signs of peripheral facial nerve palsy [25]. Disorders of the facial nerve are relatively common and have many possible causes, each resulting in varying levels of facial asymmetry due to paralysis of the structures innervated by the facial nerve. Congenital facial palsy is present at birth and can be caused by abnormal developmental processes, disturbances of the neuromuscular junction (congenital myasthenic syndrome 9–11), myopathies, or trauma (resulting from perinatal injury, especially the use of forceps during delivery). Acquired facial nerve palsy is a result of infection, neoplasms, or neurodegeneration [24].

Bell’s Palsy

The most common acute neurological cause of facial asymmetry is Bell’s palsy. This is the most frequent condition of “peripheral lesion” of the facial nerve and accounts for about two-thirds of unifacial nerve disorders. The annual incidence rate ranges from 13 to 34 cases per 100,000 with no differences between sexes [26]. The aetiology is unknown, but in some cases it is caused by a viral infection (especially herpes simplex virus type 1 (HSV-1)) [27]. Other possible causes of Bell’s palsy are anatomical, ischemic, or inflammatory in nature or due to cold stimulation [27]. Bell’s palsy is characterised by specific clinical features: weakness involving the mouth, eye, and forehead. The symptoms often are accompanied by earache, dysgeusia, or altered facial sensation. The symptoms develop within hours to days. Steroids are recommended as a therapeutic tool. It is a benign condition, with complete or near-complete recovery in the majority of cases [25].

Central Palsy

Central facial palsy occurs as a result of damage to the cortico-nuclear tract above the nucleus of Nerve VII. The clinical manifestation includes weakness in the lower part of the face, problems with smiling, and flattening of the nasolabial fold. The most common causes of central palsy are stroke, multiple sclerosis, and tumours [28]. Stroke-related oro-facial impairment depends on the location and size of vascular lesions. Cortical lesions affecting the precentral gyrus are connected to contralateral impairment of the motor and sensory functions of the face. A stroke in the middle cerebral artery (MCA) region manifests with multiple symptoms, depending on which branches and structures are affected [29]. Isolated central facial palsy has been observed in the case of lacunar stroke located in the corona radiata or pons [30,31].

Moebius Syndrome

Moebius syndrome (MS), sometimes called the Moebius sequence, is a congenital, non-progressive uni- or bilateral facial nerve palsy associated with dysfunction of other cranial nerves, especially nerve abducens [32,33]. Both the aetiology and pathology are unknown. Some theories of the underlying intrauterine environmental factors and genetic causes have been considered. The prevalence of MS is estimated to be 1:250,000 newborns, with an equal incidence between women and men [34]. The characteristic clinical feature is secondary to the failure of the abducens and the facial nerves. Facial asymmetry and dysmorphic symptoms (microencephaly, epicanthal folds, flat nasal bridge, micrognathia, defects of the external ear, dental deficits, clinodactyly low-set thumbs) are typical features of Moebius syndrome [35,36].

Ramsay Hunt Syndrome

Ramsay Hunt syndrome (or herpes zoster oticus) is a peripheral facial nerve palsy related to a vesicular rash in the external auditory canal and the mouth [37,38]. This is the second most common atraumatic lesion of the nerve palsy. Its incidence is about 5:100,000 with a predominance in women. The condition is connected to reactivation of a latent infection of the Varicella zoster virus (VZV) in the geniculate ganglion of the facial nerve [39,40]. According to anatomical associations with abducens, vestibulocochlear, or glossopharyngeal nerves or cervical spinal nerves, other clinical features can be present, such as tinnitus, hearing loss, nausea, vomiting, vertigo, and nystagmus [40,41].

Melkersson–Rosenthal Syndrome

Melkersson–Rosenthal syndrome is a rare condition characterised by three symptoms: recurrent peripheral facial nerve palsy (uni- or bilateral), recurrent or persistent oedema of facial soft tissue, and lingua plicata (scrotal tongue) [42,43]. The symptoms may appear singly or together. The aetiology is unknown, and various factors, including genetic, inflammatory, allergic, and microbial factors, are involved. In some cases, the syndrome is genetically determined, inherited autosomal dominant, and associated with a defect in chromosome 9p11 [44]. The disease affects people in the second and third decades of life [45].

Hemifacial Spasm

Hemifacial spasm (HFS) is a neuromuscular disorder manifesting in unilateral, involuntary contractions of the facial muscles of one side of the face, innervated by the ipsilateral facial nerve [46,47]. The estimated prevalence is about 11 cases per 10,000, with a predominance in women. HFS is caused by irritation of or damage to the facial nerve of varying aetiology [48]. The most common cause is vascular compression of the facial nerve root in the brainstem. The neurovascular compression is produced by the anterior inferior arteries (AICAs), posterior inferior cerebellar arteries (PICAs), and the vertebral arteries (VAs). A hemifacial spasm can be secondary to trauma, demyelinating lesion, stroke, or mastoid or ear infection [49]. The clinical features include irregular muscle contractions in the area of the lower facial muscles, such as the orbicularis oris, mentalis, zygomaticus major, and platysma [46].

Miller Fisher Syndrome

Miller Fisher Syndrome (MFS) is an immune-related polyneuropathy, a rare variant of Guillain–Barre syndrome [50]. The estimated annual incidence is 1:1,000,000. Common clinical features include the following three symptoms: gait ataxia, areflexia, and ophthalmoplegia [51,52]. Facial nerve palsy appears in half of all patients with MFS, typically in the early phase of the disease [53]. In 85% to 90% of MFS cases, antibodies against GQ1b (a ganglioside component of the nerve) are present [54].

3.2. Developmental Disorders

3.2.1. Parry–Romberg Syndrome (PRS)

Progressive hemifacial atrophy (Parry–Romberg syndrome) is a rare degenerative craniofacial condition characterised by progressive unilateral facial atrophy affecting subcutaneous tissue, cartilage, muscles, and bone structures. The first reports of the disease were made by Caleb Hillier Parry in 1815 and Moritz Heinrich Romberg in 1846, and in 1871 Eulenberg established the term “progressive facial hemiatrophy” [55]. The condition is frequently associated with linear scleroderma, also known as en coup de sabre [56]. The prevalence is about 1:70,000, with a predominance in women [57]. The disease begins in childhood, typically during the first decade of life. The aetiology is still uncertain, although it seems to be heterogenous. Many theories have been postulated, including genetic diseases, autoimmune diseases, metabolic causes, trauma, infection, and sympathetic nervous system dysfunction. The main symptom is slow unilateral facial atrophy in the region of the trigeminal nerve, usually affecting the left side of the face. The atrophy includes the forehead, periorbital region, teeth, perioral region, mandible, and neck and can be associated with a systemic manifestation, especially neurological, ophthalmological, and dermatological symptoms. In addition, cardiac, rheumatological, infectious, endocrine, maxillofacial, and orthodontic manifestations are linked with PRS. The most common neurological complications include headache, trigeminal neuralgia, and seizures. In 10% to 35% of cases, ophthalmological disturbances can be observed. Parry–Romberg syndrome may be associated with the following maxillofacial manifestations: wasting of masticatory muscles, delayed ipsilateral tooth eruption, unilateral tongue atrophy, and jaw hypoplasia [58].

3.2.2. Asymmetric Crying Facies (ACF)

Asymmetric crying facies is a rare, congenital condition connected to unilateral hypoplasia or agenesis of muscles responsible for the movement of the mouth (the depressor anguli oris muscle, the depressor of the edge of the mouth, and the depressor of the labii inferioris) [59]. The face structure is normal during rest, but worsens when a child smiles, laughs, or cries. The abnormalities may be isolated or connected to multiple dysfunctions of cardiovascular, musculoskeletal, respiratory, gastrointestinal, central nervous, or genitourinary systems. The ACF incidence rate is estimated to be 3–8 per 1000 births, with a predominance in men and the left side of the face [60].

3.2.3. Dyke–Davidoff–Masson Syndrome

Dyke–Davidoff–Masson syndrome is congenital hemiatrophy due to a stroke in the region supplied by the middle cerebral artery (MCA) in the early stages of development of the nervous system in utero [61,62]. The syndrome has a specific radiological and clinical picture [63]. Its aetiology is unknown. The characteristic clinical features include facial asymmetry, contralateral hemiplegia or hemiparesis, mental retardation, and epilepsy (very common drug-resistant seizures) [64,65].

3.2.4. Harlequin Syndrome

Harlequin syndrome is a rare disease affecting the autonomic nervous system and characterised by unilateral dysfunction of sympathetic fibres innervating the face [66]. The disease was first described in 1988. In most cases, Harlequin syndrome is idiopathic, and sometimes secondary to a structural or iatrogenic lesion [67]. It has a predominance in women. The characteristic symptoms of the syndrome are one-sided flushing and sweating on the face and sometimes chest and arm, especially after exposure to heat, stress, or physical exertion [68].

3.2.5. Klippel–Feil Syndrome

Klippel–Feil Syndrome (KFS) is a rare condition connected to the fusion of cervical vertebrae at C2 and C3 due to abnormal segmentation of the cervical spine vertebrae in early foetal development [69,70]. The syndrome occurs in approximately 1:41,000 newborns worldwide, with a slight predominance in women. Its aetiology is unclear, and some authors suggest that it has a genetic background [71]. KFS may be associated with genes GDF6/RIPPLY1/2 and PAX2, which are important in the process of regulating segmentation and re-segmentation [72,73,74]. Characteristic clinical features include a short neck, a low hairline, and limited cervical mobility. Besides skeletal abnormalities (Sprengel deformity, ribs defects, scoliosis, spina bifida), deafness, congenital heart disease, and gastrointestinal, respiratory system, and urinary disorders may be present [75,76]. A shortened neck can cause differences between the size and shape on both sides of the face. Asymmetry in the orbital area, a deficient midface, ptosis, and a lack of eyebrows have been observed. In some cases, underdeveloped low-set ears coexist with facial asymmetry [77].

3.2.6. CHARGE Syndrome

CHARGE syndrome is a genetic syndrome associated with heterogenous pathogenic variants in the gene CHD7 at chromosome locus 8q12, which encodes a protein that contains several helicase family domains [78,79]. Most cases are sporadic, but in rare cases it is inherited autosomal dominant [80]. The incidence rate is about 1:100,000 among newborns worldwide without a gender predominance. In 1979, Hall and Hittner independently made the first description of the disease; therefore, CHARGE syndrome was previously named Hall and Hittner syndrome [81]. CHARGE is an abbreviation of the following common features: coloboma, heart defects, choanal atresia, retarded growth and development, genital and/or urinal abnormalities, and ear abnormalities. The phenotype is variable and depends on the affected organs [82]. Abnormalities in the facial region account for 39% of patients with the CHARGE and CHD7 mutation [83]. Facial nerve palsy (especially on the right side of the face) is found in 32–50% of those with CHARGE syndrome [84]. In addition, craniofacial and dental anomalies (such as oligodontia or delayed eruption of teeth) are also typical features found in patients with CHARGE syndrome. Dysfunction in the cranial nerves, especially I, V, VII, VIII, IX, X, and XI, is a typical symptom and found in 70–92% of patients [84,85]. A patient with CHARGE syndrome has a typically square-shaped face with a narrow bifrontal diameter, a prominent nasal bridge, a cleft lip, small nostrils, a small mouth, and a small chin. Abnormal ear structures are a characteristic observed in 95–100% of cases. The external malformations of the ear include low-set, wide, anteverted, and cup-shaped pinnae with small or absent lobules [86]. Facial nerve palsy (uni- or bilateral) coexisting with ear abnormalities leads to significant facial asymmetry.

3.2.7. HOXA1 Syndromes: Athabascan Brain Stem Dysgenesis Syndrome (ABDS) and Bosley–Salih–Alorainy Syndrome (BSAS)

Both of these syndromes are very rare, autosomal-recessive conditions caused by a mutation in the HOXA-1 gene and abnormal brainstem functions. Most commonly, abnormalities of the eye, ear, and cardiovascular system are observed [87]. Approximately 20% of patients with HOXA-1 syndromes have congenital bilateral facial nerve palsy [88].

3.2.8. Isolated Hereditary Congenital Facial Paresis (HCFP)

This is a rare, congenital, nonprogressive, uni- or bilateral, and isolated condition involving dysfunction of the facial nerve [89]. The disease belongs to a group of conditions named congenital cranial dysinnervation disorders (CCDDs) [90]. Most of the described cases have an autosomal dominant pattern. The genetic loci of type 1 (HCFP1) are located on chromosome 3q and those of type 2 (HCFP2) have been mapped on chromosome 10q. HCFP type 3 is caused by mutation in the HOXB1 gene [91]. The condition may be associated with additional clinical manifestations, such as hearing loss, orofacial anomalies, limb malformations, and musculoskeletal system defects [92,93].

3.3. Myopathies

3.3.1. Facioscapulohumeral Muscular Dystrophy

Facioscapulohumeral muscular dystrophy (FSHMD) is the third most common type of muscular dystrophy. It is an inherited, autosomal dominant disorder characterised by a slowly progressing weakness of the muscles [94,95]. The disease is caused by mutations in DUX4 [96]. The classical clinical picture includes weakness of the facial muscles, shoulder girdles, and upper arms, followed by weakness of the trunk and limb muscles in the later course of the disease. Asymmetrical facial muscle weakness is one of the first and most characteristic symptoms of FSHD [97]. The most frequently affected muscles are the orbicularis oculi, orbicularis oris, and zygomaticus major [97,98]. The level of facial asymmetry differs from patient to patient, from discrete symptoms to myopathic facies [99].

3.3.2. Titinopathy

Titinopathy refers to various myopathies associated with mutations in the titin (TTN) gene [100]. Titin plays an important role in the function of sarcomeres [101]. The group of disorders connected to TTN mutations includes a hereditary myopathy with early respiratory failure and late-onset tibial muscular dystrophy [102]. Typically, patients present with symptoms of limb muscle weakness and problems with the heart and respiratory system [103,104]. In 70% of cases, mild to moderate facial weakness is observed. Asymmetric facial weakness and ptosis occur in 33% of patients with mutations in the TTN gene [104].

3.3.3. Myotonic Dystrophy (MD) Type 1

Myotonic dystrophy (or Steinert’s disease) is the most common type of muscular dystrophy in adults [105,106]. This is an autosomal-dominant neuromuscular disease caused by trinucleotide expansion of CTG in the noncoding region of the myotonic dystrophy protein kinase (DMPK) gene on chromosome 19q13. Its prevalence is about 1:300. MD is a multisystem condition that affects not only the musculoskeletal system but also the cardiovascular, respiratory, ophthalmological, and endocrine systems. Congenital MD is characterised by generalised weakness, including facial weakness, hypotonia, positional malformation, and respiratory problems [107]. Patients have a very characteristic facial appearance, which includes a long, thin face with ptosis, hollowing of the temples due to wasting of the temporalis muscle, and atrophy of the jaw muscles [108].

3.3.4. Carey–Fineman–Ziter Syndrome (CFZS)

This is a rare, autosomal-recessive myopathy associated with mutations in the MYMK gene, which encodes the myomaker protein (mymk) [109]. Myomaker is a plasma membrane protein responsible for myoblast fusion in the skeletal muscle [110]. Carey–Fineman–Ziter syndrome is characterised by a wide spectrum of symptoms, which mainly include a combination of the Moebius sequence and the Pierre Robin sequence associated with hypotonia, facial anomalies, and other malformations [111]. Facial abnormalities include micrognathia, a nose with a broad base, epicanthus, a thin upper lip, and abnormal pinnae.

3.3.5. Nemaline Myopathy

This is a group of congenital myopathies characterised by rod-shaped structures (nemaline rods) in a muscle biopsy [112,113]. The prevalence is about 1:22,480, with the age of onset ranging from neonates to adults [114]. The group of nemaline myopathies are genetically heterogenous. In most cases, it is autosomal dominant and associated with a mutation in the α-actin 1 (ACTA-1) gene or an autosomal-recessive mutation of nebulin (NEB) [115]. Typically, patients present with general muscle weakness, dominant in the face, neck, and proximal part of the limb connected with hypotonia. In forms connected with ACTA-1 mutations, facial weakness may be present [116]. The clinical features include an elongated face with retrognathia of the jaw (a displaced jaw that is farther back than normal) and a high palate.

3.4. Headache

3.4.1. Cluster Headache

Cluster headache is one of the trigeminal autonomic cephalgias (TCAs). It is a primary headache characterised by unilateral pain associated with ipsilateral cranial autonomic features [117]. A cluster headache typically occurs with circannual and circadian periodicity. The prevalence is about 0.1%. A cluster headache is a unilateral, severe pain mainly located around the orbital and temporal regions. The pain has a sudden onset and cessation. Accompanying symptoms include migraine symptoms, such as nausea, vomiting, photophobia, and phonophobia. Typical unilateral autonomic symptoms include ptosis, miosis, lacrimation, conjunctival injection, rhinorrhoea, and nasal congestion [118].

3.4.2. Masticatory Muscles Headache

Temporomandibular disorders (TMDs) include various conditions associated with the masticatory muscles, temporomandibular joints, and collateral structures [119,120,121]. TMDs are very common in the general population and especially affect young people between the ages of 20 and 30 years, with a predominance in women. Patients who suffer from headaches secondary to a TMD very often have asymmetry of the face [122]. Problems with TMDs can be associated with asymmetry of the facial muscles [123]. Facial asymmetry may be a result of a unilateral derangement of the temporomandibular joint, especially changes in the height of mandibular condyles, condylar or hemi-mandibular hypertrophy, or a post-trauma lesion [124,125,126].

4. Discussion

Pathological asymmetry refers to a situation with a noticeable disproportion between the two sides of the face. Dentofacial asymmetry may be present along with Class I or Class II malocclusions, but it most commonly occurs in cases with Class III malocclusions [127,128] The available data suggest a difference in facedness between males and females [129]. Males have a larger area on the left side compared with the right side, unlike women, who have a right side that is larger than the left side [129]. Studies have found differences between both parts of the face. According to the literature, the right hemiface is wider than the left hemiface [130,131]. Ercan et al. found that the left side of the face was most commonly dominant in both sexes and the most asymmetric part of the face in both sexes was the middle third of the face (the maxillary bone, the zygomatic corner, and the lower orbital border) [132]. Based on the literature, differences in the degree of facial asymmetry between different areas of the face have been reported. Ercan et al. and Haraguchi et al. found that the asymmetry in the lower third of the face was greater than in the middle and upper thirds of the face [131,133]. Facial asymmetry is very common in the general population. The prevalence of facial asymmetry ranges from 21% to 85% [134]. In a group of orthodontic patients, asymmetry ranged from 12% to 37% [135,136]. The variation in the prevalence depends on the dental–facial deformity type, the assessment methods and tools, and the criteria defining asymmetry used by the authors. Facial asymmetry may have various causes [137] and its classifications are based on various criteria [137,138]. Cheong and Lo divided the aetiology into three main groups: congenital, developmental, and acquired causes [139]. Congenital or prenatal defects are present at birth and are the result of abnormal growth of the face and abnormal facial muscles. Congenital abnormalities can be classified into malformations, deformations, and disruptions. The defects associated with facial asymmetry include a cleft lip or a cleft palate, craniosynostosis, hemifacial microsomia, anatomical changes at the base of the skull, congenital muscular torticollis, genetic conditions, vascular abnormalities, and positional plagiocephaly. Idiopathic asymmetry is considered to be developmental because the causes are unknown. The acquired conditions responsible for asymmetry include trauma, fractures, temporomandibular joint ankylosis, and tumours [140]. Bishara et al. reported four structural causes of asymmetry: dental, muscular, skeletal, and functional [141]. Dental aetiology is secondary to local factors, such as early loss of deciduous teeth, a congenital lack of teeth, or habits such as sucking one’s thumb. Asymmetry also can be due to abnormally shaped dental arches. Facial disproportion could be the result of muscular asymmetry. The deviation and abnormal growth of the mandible or maxilla are causes of skeletal asymmetry. Functional asymmetry becomes apparent when facial muscles are activated [142]. In addition, neurological disturbances can lead to facial asymmetry. Cranial nerve disorders present with varying levels of facial dysfunction. Many cranial nerve disorders exist; however, vascular lesions, traumas, and tumours are most common. The core categories of congenital facial weakness and asymmetry include myopathic and developmental problems.

5. Conclusions

Slight asymmetry of the face is a naturally occurring phenomenon. Clinically significant facial asymmetry is aetiologically and pathogenetically heterogenous. In the literature, several factors have been reported to cause asymmetry. The neurological view is different from the dental point of view. This narrative review has highlighted the impact of neurological disturbances on facial asymmetry. To the best our knowledge, this is the first review of neurological causes of facial asymmetry. Neurological problems, especially those dependent on the facial nerve, are responsible for facial asymmetry. In conclusion, this review has shown that facial asymmetry has multiple neurological aetiologies. Medical history, physical examination, and additional testing as indicated are necessary to arrive at the correct diagnosis. Complete knowledge of the aetiological factors and the character of the asymmetry plays a crucial role in formulating a treatment plan.

Author Contributions

Conceptualisation, J.C.-Ł.; writing—review and editing and supervision, B.P. All authors have read and agreed to the published version of the manuscript.


This work was supported by the Ministry of Health subventions according to No. SUBZ.C220.22.102 from the IT Simple System of the Wroclaw Medical University.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Conflicts of Interest

The authors declare no conflict of interest.


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Figure 1. The process of data collection.
Figure 1. The process of data collection.
Symmetry 14 00737 g001
Table 1. The most common neurological causes of asymmetry.
Table 1. The most common neurological causes of asymmetry.
cranial nervesoculomotor nerve
trochlear nerve
trigeminal nerve
facial nerve
developmental disordersParry–Romberg syndrome (PRS)
Asymmetric crying facies (ACF)
Dyke–Davidoff–Masson syndrome
Harlequin syndrome
Klippel–Feil syndrome
CHARGE syndromeHOXA1 syndromes
Isolated Hereditary Congenital Facial Paresis (HCFP)
myopathiesFacioscapulohumeral muscular dystrophy
Myotonic dystrophy (MD) type 1
Nemaline myopathy
Carey–Fineman–Ziter syndrome (CFZS)
headachecluster headache
masticatory muscles headache
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Chojdak-Łukasiewicz, J.; Paradowski, B. Facial Asymmetry: A Narrative Review of the Most Common Neurological Causes. Symmetry 2022, 14, 737.

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Chojdak-Łukasiewicz J, Paradowski B. Facial Asymmetry: A Narrative Review of the Most Common Neurological Causes. Symmetry. 2022; 14(4):737.

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Chojdak-Łukasiewicz, Justyna, and Bogusław Paradowski. 2022. "Facial Asymmetry: A Narrative Review of the Most Common Neurological Causes" Symmetry 14, no. 4: 737.

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