Management of AOS is largely symptomatic and aimed at treating the various congenital anomalies present in the individual. When the scalp and/or cranial bone defects are severe, early surgical intervention with grafting is indicated.

The overall prognosis is excellent in most cases. Most children with Adams–Oliver syndrome can likely expect to have a normal life span. However, individuals with more severe scalp and cranial defects may experience complications such as hemorrhage and meningitis, leading to long-term disability.

With appropriate treatment and management, patients with Weaver syndrome appear to do well, both physically and intellectually, throughout their life and have a normal lifespan. Their adult height is normal as well.

There is no cure available for Weaver syndrome. However, with multidisciplinary management such as neurological, pediatric, orthopedic, and psychomotor care and genetic counseling, symptoms can be managed. Surgery may be used to correct any skeletal issues. Physical and occupational therapy are considered an option to help with muscle tone. Also, speech therapy is often recommended for speech related problems.

There does not yet exist a specific treatment for IP. Treatment can only address the individual symptoms.

There is no known cure for Ehlers–Danlos syndrome. Treatment is palliative. Close monitoring of the cardiovascular system, physiotherapy, occupational therapy, and orthopedic instruments (e.g., wheelchairs, bracing, casting) may be helpful. This can help with stabilizing the joints and prevent injury. Orthopedic instruments are helpful for the prevention of further joint damage, especially for long distances, although it is advised that individuals not become entirely dependent on them until there are no other options for mobility. One should avoid activities that cause the joint to lock or overextend.

A physician may prescribe casting to stabilize joints. Physicians may refer a patient to an orthotist for orthotic treatment (bracing). Physicians may also consult a physical and/or occupational therapist to help strengthen muscles and to teach people how to properly use and preserve their joints.

There are different types of physiotherapy. Aquatic therapy promotes muscular development and coordination. With manual therapy, the joint will be gently mobilized within the range of motion and/or manipulations.

If conservative therapy is not helpful, surgical repair of joints may be necessary. Medication to decrease pain or manage cardiac, digestive, or other related conditions may be prescribed. To decrease bruising and improve wound healing, some patients have responded to ascorbic acid (vitamin C). Special precautions are often taken by medical care workers because of the sheer amount of complications that tend to arise in EDS patients. In Vascular EDS, signs of chest or abdominal pain are to be considered trauma situations.

In general, medical intervention is limited to symptomatic therapy. Before pregnancy, patients with EDS should have genetic counseling and familiarize themselves with the risks to their own bodies that pregnancy poses. Children with EDS should be provided with information about the disorder so they can understand why contact sports and other physically stressful activities should be avoided. Children should be taught early on that demonstrating the unusual positions they can maintain due to loose joints should not be done as this may cause early degeneration of the joints. Patients may find it hard to cope with the drawbacks of the disease. In this case, emotional support and behavioral and psychological therapy can be useful. Support groups can be immensely helpful for patients dealing with major lifestyle changes and poor health. Family members, teachers, and friends should be informed about EDS so they can accept and assist the child.

There is no 'cure' for this condition and currently, medical treatment is limited to plastic surgery with excision of the folds by means of scalp reduction/surgical resection. Scalp subcision has also been suggested as a treatment. Additional suggestions also include injections of a dermal filler i.e. Sculptra (poly-L-lactic acid)

Beare–Stevenson cutis gyrata syndrome is so rare that a reliable incidence cannot be established as of yet; fewer than 20 patients with the condition have been reported.

Lenz–Majewski syndrome is a skin condition characterized by hyperostosis, craniodiaphyseal dysplasia, dwarfism, cutis laxa, proximal symphalangism, syndactyly, brachydactyly, mental retardation, enamel hypoplasia, and hypertelorism.

In 2013, whole-exome sequencing showed that a missense mutation resulting in overactive phosphatidylserine synthase 1 was the cause of LMS, making it the first known human disease to be caused by disrupted phosphatidylserine metabolism. The researchers suggested a link between the condition and bone metabolism.

The instability of joints, leading to (sub)luxations and joint pain, often require surgical intervention in patients with Ehlers–Danlos syndrome. Instability of almost all joints can happen but appear most often in the lower and upper extremities, with the wrist, fingers, shoulder, knee, hip, and ankle being most common.

Common surgical procedures are joint debridement, tendon replacements, capsulorraphy, and arthroplasty. Studies have shown that after surgery, degree of stabilization, pain reduction, and patient satisfaction can improve, but surgery does not guarantee an optimal result: Patients and surgeons report being dissatisfied with the results. Consensus is that conservative treatment is more effective than surgery, particularly since patients have extra risks of surgical complications due to the disease. Three basic surgical problems arise due to EDS: the strength of the tissues is decreased, which makes the tissue less suitable for surgery; the fragility of the blood vessels can cause problems during surgery; and wound healing is often delayed or incomplete. If considering surgical intervention, it would be prudent to seek care from a surgeon with extensive knowledge and experience in treating patients with EDS and joint hypermobility issues.

Studies have shown that local anesthetics, arterial catheters and central venous catheters cause a higher risk in haematoma formation in patients with Ehlers–Danlos syndrome. Ehlers–Danlos syndrome patients also show a resistance to local anaesthetics. Resistance to Xylocaine and Bupivacaine is not uncommon, and Carbocaine tends to work better in EDS patents. Special recommendations for anesthesia in EDS patients are prepared by orphananesthesia and deal with all aspects of anesthesia for people with EDS. Detailed recommendations for anesthesia and perioperative care of patients with EDS should be used to improve patient safety.

Surgery with Ehlers–Danlos patients requires careful tissue handling and a longer immobilization afterward.

There is no cure for this condition. Treatment is supportive and varies depending on how symptoms present and their severity. Some degree of developmental delay is expected in almost all cases of M-CM, so evaluation for early intervention or special education programs is appropriate. Rare cases have been reported with no discernible delay in academic or school abilities.

Physical therapy and orthopedic bracing can help young children with gross motor development. Occupational therapy or speech therapy may also assist with developmental delays. Attention from an orthopedic surgeon may be required for leg length discrepancy due to hemihyperplasia.

Children with hemihyperplasia are thought to have an elevated risk for certain types of cancers. Recently published management guidelines recommend regular abdominal ultrasounds up to age eight to detect Wilms' tumor. AFP testing to detect liver cancer is not recommended as there have been no reported cases of hepatoblastoma in M-CM patients.

Congenital abnormalities in the brain and progressive brain overgrowth can result in a variety of neurological problems that may require intervention. These include hydrocephalus, cerebellar tonsillar herniation (Chiari I), seizures and syringomyelia. These complications are not usually congenital, they develop over time often presenting complications in late infancy or early childhood, though they can become problems even later. Baseline brain and spinal cord MRI imaging with repeat scans at regular intervals is often prescribed to monitor the changes that result from progressive brain overgrowth.

Assessment of cardiac health with echocardiogram and EKG may be prescribed and arrhythmias or abnormalities may require surgical treatment.

Prognosis varies widely depending on severity of symptoms, degree of intellectual impairment, and associated complications. Because the syndrome is rare and so newly identified, there are no long term studies.

Zori–Stalker–Williams syndrome, also known as pectus excavatum, macrocephaly, short stature and dysplastic nails, is a rare autosomal dominant congenital disorder associated with a range of features such as pectus excavatum, macrocephaly and dysplastic nails, familial short stature, developmental delay and distinctive facies. Further signs are known to be associated with this syndrome.

The name originates from the researchers who first defined and noticed the syndrome and its clinical signs.

It is believed that the syndrome is inherited in an autosomal dominant pattern, though there has been no new research undertaken for this rare disease.

Gerodermia osteodysplastica (GO), also called geroderma osteodysplasticum and Walt Disney dwarfism, is a rare autosomal recessive connective tissue disorder included in the spectrum of cutis laxa syndromes.

Usage of the name "Walt Disney dwarfism" is attributed to the first known case of the disorder, documented in a 1950 journal report, in which the authors described five affected members from a Swiss family as having the physical appearance of dwarves from a Walt Disney film.

The terms "geroderma" or "gerodermia" can be used interchangeably with "osteodysplastica" or "osteodysplasticum", with the term "hereditaria" sometimes appearing at the end.

Treatment of manifestations: special hair care products to help manage dry and sparse hair; wigs; artificial nails; emollients to relieve palmoplantar hyperkeratosis.

Focal facial dermal dysplasia (FFDD) is a rare genetically heterogeneous group of disorders that are characterized by congenital bilateral scar like facial lesions, with or without associated facial anomalies. It is characterized by hairless lesions with fingerprint like puckering of the skin, especially at the temples, due to alternating bands of dermal and epidermal atrophy.

This condition is also known as Brauer syndrome (hereditary symmetrical aplastic nevi of temples, bitemporal aplasia cutis congenita, bitemporal aplasia cutis congenita: OMIM ) and Setleis syndrome (facial ectodermal dysplasia: OMIM ).

Several mutations in the FGFR2 gene (a gene coding for a protein called fibroblast growth factor receptor 2, which is involved in important signaling pathways) are known to cause Beare–Stevenson cutis gyrata syndrome; however, not all patients with the condition have a mutation in their FGFR2 gene. Any alternative underlying causes are currently unidentified. The syndrome follows an autosomal dominant pattern, meaning that if one of the two available genes carries a mutation the syndrome will result. Currently, no familial histories are known (in other words, there are no reports of cases in which a parent carrying a mutation in their FGFR2 gene then propagated said mutation to his or her child).

Aplasia cutis congenita (ACC) is a rare disorder characterized by congenital absence of skin. Frieden classified ACC in 1986 into 9 groups on the basis of location of the lesions and associated congenital anomalies. The scalp is the most commonly involved area with lesser involvement of trunk and extremities. Frieden classified ACC with fetus papyraceus as type 5. This type presents as truncal ACC with symmetrical absence of skin in stellate or butterfly pattern with or without involvement of proximal limbs.]It is the most common congenital cicatricial alopecia, and is a congenital focal absence of epidermis with or without evidence of other layers of the skin.

The exact etiology of ACC is still unclear but intrauterine infection by varicella or herpes virus, drugs such as methimazole, misoprostol, valproate, cocaine, marijuana etc., fetus papyraceus, feto-fetal transfusion, vascular coagulation defects, amniotic membrane adherence, abnormal elastic fiber biomechanical forces and trauma are implicated. It can be associated with Johanson-Blizzard syndrome, Adams-Oliver syndrome, trisomy 13, and Wolf-Hirschhorn syndrome.

It can also seen with exposure to methimazole and carbimazole in utero. This dermatological manifestation has been linked to Peptidase D haploinsufficiency and a deletion in Chromosome 19.

Many features of gerodermia osteodysplastica (GO) and another autosomal recessive form of cutis laxa, wrinkly skin syndrome (WSS, ""), are similar to such an extent that both disorders were believed to be variable phenotypes of a single disorder.

Several delineating factors, however, suggest that gerodermia osteodysplastica and wrinkly skin syndrome are distinct entities, but share the same clinic spectrum.

While the prevailing feature of wrinkly, loose skin is more localized with GO, it is usually systemic, yet eases in severity with age during the course of WSS. Also, as the fontanelles ("soft spots") are usually normal on the heads of infants with GO, they are often enlarged in WSS infants.

While WSS is associated with mutations of genes on chromosomes 2, 5, 7, 11 and 14; GO has been linked to mutations in the protein GORAB. A serum sialotransferrin type 2 pattern, also observed with WSS, is not present in GO patients.

But perhaps the most notable feature, differentiating GO from WSS and similar cutis laxa disorders, is the age-specific metaphyseal peg sometimes found in GO-affected long bone, near the knee. Not appearing until around age 4–5, then disappearing by physeal closure, this oddity of bone is thought to represent a specific genetic marker unique to GO and its effects on bone development.

Watson syndrome is an autosomal dominant condition characterized by Lisch nodules of the ocular iris, axillary/inguinal freckling, pulmonary valvular stenosis, relative macrocephaly, short stature, and neurofibromas.

Watson syndrome is allelic to NF1, the same gene associated with neurofibromatosis type 1.

Cutis laxa (also known as chalazoderma, dermatochalasia, dermatolysis, dermatomegaly, generalized elastolysis, generalized elastorrhexis, or pachydermatocele) is a group of rare connective tissue disorders in which the skin becomes inelastic and hangs loosely in folds.

This condition has been linked to mutations in the ribosomal GTPase BMS1 gene.

Patterson syndrome, also called pseudoleprechaunism, is an extremely rare syndrome, first mistaken as Donohue Syndrome (also known as Leprechaunism).

It is named for Dr. Joseph Hanan Patterson. It was described by Patterson and Watkins in 1962.

The pathogenesis and cause of the Patterson syndrome was unknown until 1981.

Treatment is symptomatic. There is no standard course of treatment for Sotos syndrome.

Woodhouse–Sakati syndrome, also called hypogonadism, alopecia, diabetes mellitus, intellectual disability and extrapyramidal syndrome, is a rare autosomal recessive multisystem disorder which causes malformations throughout the body, and deficiencies affecting the endocrine system.