Treatment for MSS is symptomatic and supportive including physical and occupational therapy, speech therapy, and special education. Cataracts must be removed when vision is impaired, generally in the first decade of life. Hormone replacement therapy is needed if hypogonadism is present.

Treatment is aimed at managing the symptoms of the disease. A form of laser eye surgery named keratectomy may help with the superficial corneal scarring. In more severe cases, a partial or complete corneal transplantation may be considered. However, it is common for the dystrophy to recur within the grafted tissue.

The treatment for Morquio syndrome consists of prenatal identification and of enzyme replacement therapy. On 12 February 2014, the US Food and Drug Administration approved the drug elosulfase alfa (Vimizim) for treating the disease.

Treatment is not needed in the asymptomatic patient. Symptomatic patients may benefit from surgical debulking of the tumor. Complete tumor removal is not usually needed and can be difficult due to the tumor location.

Early stages may be asymptomatic and may not require any intervention. Initial treatment may include hypertonic eyedrops and ointment to reduce the corneal edema and may offer symptomatic improvement prior to surgical intervention.

Suboptimal vision caused by corneal dystrophy usually requires surgical intervention in the form of corneal transplantation. Penetrating keratoplasty, a common type of corneal transplantation, is commonly performed for extensive corneal dystrophy.

With penetrating keratoplasty (corneal transplant), the long-term results are good to excellent. Recent surgical improvements have been made which have increased the success rate for this procedure. However, recurrence of the disease in the donor graft may happen. Superficial corneal dystrophies do not need a penetrating keratoplasty as the deeper corneal tissue is unaffected, therefore a lamellar keratoplasty may be used instead.

Phototherapeutic keratectomy (PTK) can be used to excise or ablate the abnormal corneal tissue. Patients with superficial corneal opacities are suitable candidates for a this procedure.

The preferred treatment of congenital glaucoma is surgical not medical. The initial procedures of choice are goniotomy or trabeculotomy if the cornea is clear, and trabeculectomy ab externo if the cornea is hazy. The success rates are similar for both procedures in patients with clear corneas. Trabeculectomy and shunt procedures should be reserved for those cases in which goniotomy or trabeculotomy has failed. Cyclophotocoagulation is necessary in some intractable cases but should be avoided whenever possible because of its potential adverse

effects on the lens and the retina.

Corneal transplant is not needed except in very severe and late cases.

Light sensitivity may be overcome by wearing tinted glassess.

There is no standard course of treatment for cerebellar hypoplasia. Treatment depends upon the underlying disorder and the severity of symptoms. Generally, treatment is symptomatic and supportive. Balance rehabilitation techniques may benefit those experiencing difficulty with balance. Treatment is based on the underlying disorder and the symptom severity. Therapies include physical, occuptational, speech/language, visual, psych/ behavioral meds, special education.

Reis-Bücklers corneal dystrophy is not associated with any systemic conditions.

Phototherapeutic keratectomy (PTK) done by an ophthalmologist can restore and preserve useful visual function for a significant period of time in patients with anterior corneal dystrophies including EBMD.

There is no known cure for MSA and management is primarily supportive.

Ongoing care from a neurologist specializing in "movement disorders" is recommended as the complex symptoms of MSA are often not familiar to less-specialized health care professionals.

One particularly serious problem, the drop in blood pressure upon standing up (with risk of fainting and thus injury from falling) often responds to fludrocortisone, a synthetic mineralocorticoid. Another common drug treatment is midodrine (an alpha-agonist). Non-drug treatments include "head-up tilt" (elevating the head of the whole bed by about 10 degrees), salt tablets or increasing salt in the diet, generous intake of fluids, and pressure (elastic) stockings. Avoidance of triggers of low blood pressure (such as hot weather, alcohol, and dehydration) are crucial.

Hospice/homecare services can be very useful as disability progresses.

Levodopa (L-Dopa), a drug used in the treatment of Parkinson's disease, improves parkinsonian symptoms in a small percentage of MSA patients. A recent trial reported that only 1.5% of MSA patients experienced a less than 50% improvement when taking levodopa, and even this was a transient effect lasting less than one year. Poor response to L-Dopa has been suggested as a possible element in the differential diagnosis of MSA from Parkinson's disease.

A November, 2008 study conducted in Europe failed to find an effect for the drug riluzole in treating MSA or PSP.

Management by rehabilitation professionals (physiatrists, physiotherapists, occupational therapists, speech therapists, and others) for problems with walking/movement, daily tasks, and speech problems is essential.

Physiotherapy can help to maintain the patient’s mobility and will help to prevent contractures. Instructing patients in gait training will help to improve their mobility and decrease their risk of falls. A physiotherapist may also prescribe mobility aids such as a cane or a walker to increase the patient’s safety. Other ways a physiotherapist can help to improve the patient’s safety are to teach them to move and transfer from sitting to standing slowly to decrease risk of falls and limit the effect of postural hypotension. Instruction in ankle pumping helps to return blood in the legs to the systemic circulation. To further control the postural hypotension, raising the head of the bed by 8 in (20.3 cm) while sleeping may be indicated as well as the use of elastic compression garments.

Speech and language therapists may assist in assessing, treating and supporting speech (dysarthria) and swallowing difficulties (dysphagia). Early intervention of swallowing difficulties is particularly useful to allow for discussion around tube feeding further in the disease progression.{doubtful - citation needed} At some point in the progression of the disease, fluid and food modification may be suggested. Speech changes mean that alternative communication may be needed, for example communication aids or word charts.

Social workers and occupational therapists can also help with coping with disability through the provision of equipment and home adaptations, services for caregivers and access to healthcare services, both for the person with MSA as well as family caregivers.

Treatment for individuals with Dandy–Walker Syndrome generally consists of treating the associated problems, if needed.

A special tube (shunt) to reduce intracranial pressure may be placed inside the skull to control swelling. Endoscopic third ventriculostomy is also an option.

Treatment may also consist of various therapies such as occupational therapy, physiotherapy, speech therapy or specialized education. Services of a teacher of students with blindness/visual impairment may be helpful if the eyes are affected.

Ataxia usually goes away without any treatment. In cases where an underlying cause is identified, your doctor will treat the underlying cause. In extremely rare cases, you may have continuing and disabling symptoms. Treatment includes corticosteroids, Intravenous immunoglobulin, or plasma exchange therapy. Drug treatment to improve muscle coordination has a low success rate. However, the following drugs may be prescribed: clonazepam, amantadine, gabapentin, or buspirone. Occupational or physical therapy may also alleviate lack of coordination. Changes to diet and nutritional supplements may also help. Treatment will depend on the cause. If the acute cerebellar ataxia is due to bleeding, surgery may be needed. For a stroke, medication to thin the blood can be given. Infections may need to be treated with antibiotics. Steroids may be needed for swelling (inflammation) of the cerebellum (such as from multiple sclerosis). Cerebellar ataxia caused by a recent viral infection may not need treatment.

Treatment is supportive.

- The aplastic anemia and immunodeficiency can be treated by bone marrow transplantation.

- Supportive treatment for gastrointestinal complications and infections.

- Genetic counselling.

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.

Supportive treatment is the only intervention for acute cerebellar ataxia of childhood. Symptoms may last as long as 2 or 3 months.

Corneal-cerebellar syndrome (also known as Der Kaloustian-Jarudi-Khoury syndrome) is an autosomally resessive disease that was first described in 1985. Three cases are known: all are sisters in the same family.

It was concluded by Mousa-Al et al. that the disease is different from a disease known as spastic ataxia-corneal dystrophy syndrome that had been found a year later in 1986 in an inbred Bedouin family. Corneal-cerebellar syndrome differs from the spastic ataxia-corneal dystrophy syndrome by causing mental retardation. Corneal dystrophy is also epithelian instead of being stromal.

Brain MRI shows vermis atrophy or hypoplasic. Cerebral and cerebellar atrophy with white matter changes in some cases.

Spastic ataxia-corneal dystrophy syndrome (also known as Bedouin spastic ataxia syndrome) is an autosomally resessive disease. It has been found in an inbred Bedouin family. It was first described in 1986. A member of the family who was first diagnosed with this disease also had Bartter syndrome. It was concluded by its first descriptors Mousa-Al et al. that the disease is different from a disease known as corneal-cerebellar syndrome that had been found in 1985.

Symptoms include spastic ataxia, cataracts, macular corneal dystrophy and nonaxial myopia. Mental development is normal.

Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms. Myoclonus and seizures may be treated with drugs like valproate.

Some have described this condition as difficult to characterize.

The objective of irradiation is to halt the growth of the acoustic neuroma tumour, it does not excise it from the body, as the term 'radiosurgery' or 'gammaknife' implies. Radiosurgery is only suitable for small to medum size tumors.

Early diagnosis, targeted treatment according to the severity of the disease, and regular monitoring of patients with neurotrophic keratitis are critical to prevent damage progression and the occurrence of corneal ulcers, especially considering that the deterioration of the condition is often poorly symptomatic.

The purpose of treatment is to prevent the progression of corneal damage and promote healing of the corneal epithelium. The treatment should always be personalized according to the severity of the disease. Conservative treatment is typically the best option.

In stage I, the least serious, treatment consists of the administration of preservative-free artificial tears several times a day in order to lubricate and protect the ocular surface, improving the quality of the epithelium and preventing the possible loss of transparency of the cornea.

In stage II, treatment should be aimed at preventing the development of corneal ulcers and promoting the healing of epithelial lesions. In addition to artificial tears, topical antibiotics may also be prescribed to prevent possible infections. Patients should be monitored very carefully since, being the disease poorly symptomatic, the corneal damage may progress without the patient noticing any worsening of the symptoms. Corneal contact lenses can also be used in this stage of the disease, for their protective action to improve corneal healing.

In the most severe forms (stage III), it is necessary to stop the progression towards corneal perforation: in these cases, a possible surgical treatment option is tarsorrhaphy, i.e. the temporary or permanent closure of the eyelids by means of sutures or botulinum toxin injection. This protects the cornea, although the aesthetic result of these procedures may be difficult to accept for patients. Similarly, a procedure that entails the creation of a conjunctival flap has been shown to be effective in the treatment of chronic corneal ulcers with or without corneal perforation. In addition, another viable therapeutic option is amniotic membrane graft, which has recently been shown to play a role in stimulating corneal epithelium healing and in reducing vascularisation and inflammation of the ocular surface . Other approaches used in severe forms include the administration of autologous serum eye drops.

Research studies have focused on developing novel treatments for neurotrophic keratitis, and several polypeptides, growth factors and neuromediators have been proposed[25]. Studies were conducted on topical treatment with Substance P and IGF-1 (insulin-like growth factor-1), demonstrating an effect on epithelial healing[26]. Nerve Growth Factor (NGF) play a role in the epithelial proliferation and differentiation and in the survival of corneal sensory nerves. Topical treatment with murine NGF showed to promote recovery of epithelial integrity and corneal sensitivity in NK patients[27]. Recently, a recombinant human nerve growth factor eye drop formulation has been developed for clinical use[28].

Cenegermin, a recombinant form of human NGF, has recently been approved in Europe in an eye drop formulation for neurotrophic keratitis.

There are three modalities of surgical treatment (excision) depending on where the anatomical location of the incision to access the tumor is made: retrosigmoid (a variant of what was formerly called suboccipital), translabyrinthine, and middle fossa.

The goals of surgery are to control the tumor, and preserve hearing as well as facial nerves. Especially in the case of larger tumors, there may be a tradeoff between tumor removal and preservation of nerve functionality.

There are different defined degrees of surgical excision, termed 'subtotal resection', 'radical subtotal resection', 'near-total resection', and 'total resection' in order or increasing proportion of tumor removed. Lesser amount of tumor removal may increase likelihood of preservation of nerve function (hence better post-operative hearing), but also likelihood of tumor regrowth, necessitating additional treatment.