What Is Moebius Syndrome?

As a very simple explanation, Moebius syndrome is a form of facial paralysis combined with outward, to the side, eye paralysis. Individuals with Moebius syndrome typically cannot make facial expressions, such as smiling, frowning, squinting, or blinking. Speech, eating, and lip movement may also be affected. People with Moebius syndrome also cannot move their eyes out to the side, as you would if you were looking over your shoulder without turning your head. The syndrome has a wide range of presentations and may occur on one or both sides of the face. 

What Is Moebius Syndrome?

Moebius syndrome is a congenital (present at birth), non-progressive facial weakness with limited outward horizontal movement of one or both eyes. An additional criterion of having full vertical (up and down) eye movement, prior to any eye surgery, has also been suggested.

Congenital facial weakness and the inability to abduct (move the eye away from the nose) in one or both eyes, must be present for a diagnosis of Moebius syndrome. These two symptoms may be due to the underdevelopment or absence of the facial nerve (cranial nerve 7) and the abducens nerve (cranial nerve 6), respectively.

Facial weakness caused by Moebius syndrome may present on one (unilateral) or both (bilateral) sides of the face.

Moebius syndrome may affect other cranial nerves (typically the lower ones, such as nerves 9, 11, and 12) in addition to nerves 6 and 7. Learn more about the 12 cranial nerves.

Cranial Nerves Image

Additional Clinical Presentations

Moebius syndrome may occur with other clinical symptoms, including: 

  • Strabismus (cross-eyes or misalignment of the eyes), which may develop over time and not be present at birth
  • Hearing loss
  • Club foot
  • Limb differences (hand, foot, or other limb anomalies)
  • Muscular hypotonia (low muscle tone)
  • Congenital heart disease
  • Developmental delays (delayed timing to reach milestones such as independent sitting, walking, and/or speech)
  • Autism
  • Dental concerns
  • Sleep disorders
  • Poland syndrome (an underdeveloped chest wall muscle, webbed fingers, and a small hand)

In most cases of Moebius syndrome, cognitive development is typical. When intellectual disability is present, affected persons tend to have additional clinical features such as congenital heart disease, cleft palate, and other systemic (body-wide) involvement and symptoms.


Similar Facial Palsy Conditions

Genetic research into Moebius syndrome has identified other genetic conditions with clinical features overlapping with that of Moebius syndrome. They are:

  • Mutations in the gene named TUBB3: In addition to congenital facial palsy, TUBB3 presents with both restricted vertical gaze and limited horizontal eye movement. Persons diagnosed with a TUBB3 mutation have ptosis, or droopiness of the eyelids.
  • Carey-Fineman Ziter syndrome: Includes facial weakness, full eye movements, and cleft palate with a small chin (Pierre-Robin sequence), and/or hypotonia (muscle weakness). This syndrome is due to changes in the gene named MYMK and is a muscle condition (myopathy), not a condition of the cranial nerves.
  • STAC3 disorder (also known as Native American myopathy): This disorder presents with low muscle tone, facial weakness, contractures, and/or skeletal differences.  This disorder is also a muscle disease (myopathy) and not a condition of the cranial nerves.

This list is not inclusive of all congenital facial weakness conditions; please refer to “A Framework For the Evaluation of Patients With Congenital Facial Weakness” by Dr. Bryn D. Webb, et al. for more detailed information on the types of congenital facial weakness disorders.

Support, events, and information from the Moebius Syndrome Foundation are open to individuals with any form of congenital facial weakness, regardless of genetic cause or official diagnosis. 

Frequently Asked Questions

What is the cause of Moebius syndrome?

The cause of Moebius syndrome is not well understood. Genetic research into the condition has not shown a clear genetic pattern.

There is no family history of Moebius syndrome and it occurs sporadically. There are some conditions with overlapping features to Moebius syndrome that may run in families, but in studies supported by the Moebius Syndrome Foundation, no individuals with classic Moebius syndrome have more than one affected family member in their families.

While some research completed in Europe, with lead authors from the Netherlands, has indicated that Moebius syndrome may occur with changes in genes PLXND1 and REV3L, researchers in the United States have been unable to identify additional patients with changes in these two genes.

Moebius syndrome-like conditions may occur from fetal exposure to drugs that cause the constriction of blood vessels. However, it is important to understand that these drugs cause a minority of cases of Moebius syndrome. 

Some medical literature has theorized that reduced blood flow, or vascular interruption, may contribute or be the cause of Moebius syndrome.

Research into the cause of Moebius syndrome is ongoing.

How often does Moebius syndrome occur?

The estimated incidence of Moebius syndrome is roughly 2 to 20 cases per 1 million births. Moebius syndrome occurs equally in all populations. The condition occurs in all ethnicities. There is no gender bias; males and females are affected equally.

Why is it called Moebius syndrome?

Moebius syndrome was originally described by German ophthalmologist Alfred Graefe in 1880, but it is named for German neurologist Paul Julius Moebius, who reported features of this condition in 1888.


Genetic Research into Moebius Syndrome, presented by Elizabeth Engle, M.D., Ethilyn Jabs, M.D., Irini Manoli, M.D., Bryn Webb, M.D. 2022 Moebius Syndrome Foundation Conference, Atlanta, GA. 

Miller, G. Neurological disorders. The mystery of the missing smile. Science 2007;316:826-7.

Picciolini O, Porro M, Cattaneo E, Castelletti S, Masera G, Mosca F, Bedeschi MF. Moebius syndrome: clinical features, diagnosis, management and early intervention. Ital J Pediatr. 2016 Jun 3;42(1):56. doi: 10.1186/s13052-016-0256-5. PMID: 27260152; PMCID: PMC4893276.

Webb BD, Manoli I, Engle EC, Jabs EW. A framework for the evaluation of patients with congenital facial weakness. Orphanet J Rare Dis. 2021 Apr 7;16(1):158. doi: 10.1186/s13023-021-01736-1. PMID: 33827624; PMCID: PMC8028830.

Webb BD, Shaaban S, Gaspar H, Cunha LF, Schubert CR, Hao K, Robson CD, Chan WM, Andrews C, MacKinnon S, Oystreck DT, Hunter DG, Iacovelli AJ, Ye X, Camminady A, Engle EC, Jabs EW. HOXB1 founder mutation in humans recapitulates the phenotype of Hoxb1-/- mice. Am J Hum Genet. 2012 Jul 13;91(1):171-9. doi: 10.1016/j.ajhg.2012.05.018. Epub 2012 Jul 5. PMID: 22770981; PMCID: PMC3397264.