If cranial nerve VIII is affected, the person experiences hearing loss.Other symptoms that sometimes occur with Möbius syndrome are:
Limb abnormalities—clubbed feet, missing fingers or toes
Chest-wall abnormalities (Poland syndrome)
Crossed eyes (strabismus)
Difficulty in breathing and/or in swallowing
Corneal erosion resulting from difficulty in blinkingChildren with Möbius syndrome may have delayed speech because of paralysis of muscles that move the lips, soft palate and tongue root. However, with speech therapy, most people with Möbius syndrome can develop understandable speech. Möbius syndrome has been associated with increased occurrence of the symptoms of autism. Some children with Möbius syndrome are mistakenly labeled as intellectually disabled because of their expressionless faces, strabismus and frequent drooling. Social and lifestyle effects
Möbius syndrome does not prevent individuals from experiencing personal and professional success. Due to the importance of facial expression and smiling in social interaction, the inability to form either can lead to individuals with Möbius being perceived as unhappy, unfriendly or uninterested in conversations. Individuals who are familiar with Möbius patients such as family or friends can recognize other signals of emotion such as body language, to the point that they sometimes report forgetting that the person has facial paralysis. Indeed, people with Möbius syndrome are often adept at compensating for a lack of expression by using body language, posture, and vocal tone to convey emotion. Pathogenesis
Möbius syndrome results from the underdevelopment of the VI and VII cranial nerves. The VI cranial nerve controls lateral eye movement, and the VII cranial nerve controls facial expression.The causes of Möbius syndrome are poorly understood.
Cutis laxa may also be seen in association with inherited connective tissue disorders such as Ehlers–Danlos syndromes. Another syndrome associated with cutis laxa is Lenz-Majewski syndrome which is due to a mutation in the phosphatidylserine synthase 1 (PTDSS1) gene.In contrast, acquired cutis laxa often has a triggering event such as urticaria, drugs (such as penicillin) or neoplasms. Acquired cutis laxa may also be immunologically mediated, as it can involve dermal deposit of immunoglobulins and it can occur with autoimmune diseases. Acquired cutis laxa has been associated with granular immunoglobulin A deposits as well as abundant neutrophils. One hypothesis for the cause is excessive elastase release from neutrophils and macrophages. It has also been considered that mutations in elastin (ELN) and fibulin-5 (FBLN5) genes can increase susceptibility of elastic fibres to inflammatory degradation in acquired cutis laxa.Acquired cutis laxa has also been seen in conjunction with a number of conditions including: rheumatoid arthritis, systemic lupus erythematosus, celiac disease, and monoclonal gammopathies. It can also occur as a postinflammatory response after urticaria. Urticarial skin fibroblasts have shown a 2- to 3- fold increase in elastase activity in a patient with acquired cutis laxa. Diagnosis
Treatment
As of 2019, there is no treatment for cutis laxa. Procedures aimed at mitigating symptoms and identifying subsequent conditions are often advised. No pharmacological  agent has been able to stop the progression of the disease. However, cosmetic surgeries are potentially an option as cutis laxa does not generally involve vascular fragility. See also
Occipital horn syndrome
List of cutaneous conditions

References
Further reading
External links

Medscape entry on Cutis Laxa