There is no known cure to BVVL however a Dutch group have reported the first promising attempt at treatment of the disorder with high doses of riboflavin. This Riboflavin protocol seems to be beneficial in almost all cases. Specialist medical advice is of course essential to ensure the protocol is understood and followed correctly.

Patients will almost certainly require additional symptomatic treatment and supportive care. This must be specifically customized to the needs of the individual but could include mobility aids, hearing aids or cochlear implants, vision aids, gastrostomy feeding and assisted ventilation, while steroids may or may not help patients.

The first report of BVVL syndrome in Japanese literature was of a woman that had BVVL and showed improvement after such treatments. The patient was a sixty-year-old woman who had symptoms such as sensorineural deafness, weakness, and atrophy since she was 15 years old. Around the age of 49 the patient was officially diagnosed with BVVL, incubated, and then attached to a respirator to improve her CO2 narcosis. After the treatments, the patient still required respiratory assistance during sleep; however, the patient no longer needed assistance by a respirator during the daytime.

As of 2010, there was no cure for MMND. People with MMND are given supportive care to help them cope, which can include physical therapy, occupational therapy, counselling, and hearing aids.

The clinical course of BVVL can vary from one patient to another. There have been cases with progressive deterioration, deterioration followed by periods of stabilization, and deterioration with abrupt periods of increasing severity.

The syndrome has previously been considered to have a high mortality rate but the initial response of most patients to the Riboflavin protocol are very encouraging and seem to indicate a significantly improved life expectancy could be achievable. There are three documented cases of BVVL where the patient died within the first five years of the disease. On the contrary, most patients have survived more than 10 years after the onset of their first symptom, and several cases have survived 20–30 years after the onset of their first symptom.

Families with multiple cases of BVVL and, more generally, multiple cases of infantile progressive bulbar palsy can show variability in age of disease onset and survival. Dipti and Childs described such a situation in which a family had five children that had Infantile PBP. In this family, three siblings showed sensorineural deafness and other symptoms of BVVL at an older age. The other two siblings showed symptoms of Fazio-Londe disease and died before the age of two.

Treatment is symptomatic and may include nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids to reduce swelling, antibiotics and immunosuppressants. Surgery may be indicated to relieve pressure on the facial nerves and reduce swelling, but its efficacy is uncertain. Massage and electrical stimulation may also be prescribed.

There is no causative / curative therapy. Symptomatic medical treatments are focussing on symptoms caused by orthopaedic, dental or cardiac problems. Regarding perioperative / anesthesiological management, recommendations for medical professionals are published at OrphanAnesthesia.

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

Canakinumab has been approved for treatment of HIDS and has shown to be effective. The immunosuppressant drugs etanercept and anakinra have also shown to be effective. Statin drugs might decrease the level of mevalonate and are presently being investigated. A recent single case report highlighted bisphosphonates as a potential therapeutic option.

People with MMND become progressively more weak with time. Generally, affected individuals survive up to 30 years after they are diagnosed.

If binocular vision is present and head position is correct, treatment is not obligatory.

Treatment is required for: visual symptoms, strabismus, or incorrect head position.

Acquired cases that have active inflammation of the superior oblique tendon may benefit from local corticosteroid injections in the region of the trochlea.

The goal of surgery is to restore free ocular rotations. Various surgical techniques have been used:

- Harold Brown advocated that the superior oblique tendon be stripped. A procedure named sheathotomy. The results of such a procedure are frequently unsatisfactory because of reformation of scar tissue.

- Tenotomy of the superior oblique tendon (with or with out a tendon spacer) has also been advocated. This has the disadvantage that it frequently produces a superior oblique paresis.

- Weakening of the inferior oblique muscle of the affected eye may be needed to compensate for iatrogenic fourth nerve palsy.

During surgery, a traction test is repeated until the eye rotations are free and the eye is anchored in an elevated adducted position for about two weeks after the surgery. This maneuver is intended to prevent the reformation of scar tissue in the same places. Normalization of head position may occur but restoration of full motility is seldom achieved. A second procedure may be required.

Berger, in 1876, first reported a case of 12-year-old child with progressive bulbar paralysis

Patients generally respond well to treatment. Iron supplementation usually resolves the anemia, and corrects the glossodynia (tongue pain).

Treatment is primarily aimed at correcting the iron-deficiency anemia. Patients with PVS should receive iron supplementation in their diet. This may improve dysphagia and pain. If not, the web can be dilated during upper endoscopy to allow normal swallowing and passage of food.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life-threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.

Café au lait spots can be removed with lasers. Results are variable as the spots are often not completely removed or can come back after treatment. Often, a test spot is treated first to help predict the likelihood of treatment success.

Onset of first symptom has been reported between 1–12 years, with a mean age of onset at 8 years. Clinical course can be divided into early (< 6 yrs age, predominance of respiratory symptoms) and late course (6–20 years of age, predominance of motor symptoms on superior limbs). Progression to involve other cranial nerve muscles occurs over a period of months or years. In the Gomez review facial nerve was affected in all cases while hypoglossal nerve was involved in all except one case. Other cranial nerves involved were vagus, trigeminal, spinal accessory nerve, abducent, occulomotor and glossopharyngeal in this order. Corticospinal tract signs were found in 2 of the 14 patients.

The disease may progress to patient's death in a period as short as 9 months or may have a slow evolution or may show plateaus. Post mortem examination of cases have found depletion of nerve cells in the nuclei of cranial nerves. The histologic alterations found in patient with Fazio–Londe disease were identical to those seen in infantile-onset spinal muscular atrophy.

Strength may improve with administration of cholinesterase inhibitors.

Lip pits may be surgically removed either for aesthetic reasons or discomfort due to inflammation caused by bacterial infections or chronic saliva excretion, though spontaneous shrinkage of the lip pits has occurred in some rare cases. Chronic inflammation has also been reported to cause squamous-cell carcinoma. It is essential to completely remove the entire lip pit canal, as mucoid cysts can develop if mucous glands are not removed. A possible side effect of removing the lip pits is a loose lip muscle. Other conditions associated with VWS, including CL, CP, congenital heart defects, etc. are surgically corrected or otherwise treated as they would be if they were non-syndromic.

In general, there is no treatment available for CMTC, although associated abnormalities can be treated. In the case of limb asymmetry, when no functional problems are noted, treatment is not warranted, except for an elevation device for the shorter leg.

Laser therapy has not been successful in the treatment of CMTC, possibly due to the presence of many large and deep capillaries and dilated veins. Pulsed-dye laser and long-pulsed-dye laser have not yet been evaluated in CMTC, but neither argon laser therapy nor YAG laser therapy has been helpful.

When ulcers develop secondary to the congenital disease, antibiotic treatment such as oxacillin and gentamicin administered for 10 days has been prescribed. In one study, the wound grew Escherichia coli while blood cultures were negative.

Megalencephalic leukoencephalopathy with subcortical cysts (MLC, or Van der Knaap disease) is a form of hereditary CNS demyelinating disease. It belongs to a group of disorders called leukodystrophies.

It is associated with MLC1. Van der Knaap disease is named after Dutch neurologist Marjo van der Knaap.

Jalili syndrome is a genetic disorder characterized by the combination of cone-rod dystrophy of the retina and amelogenesis imperfecta. It was characterized in 1988 by Dr. I. K. Jalili and Dr. N. J. D. Smith, following the examination of 29 members of an inbred, Arab family living within the Gaza Strip.

Melkersson–Rosenthal syndrome may recur intermittently after its first appearance. It can become a chronic disorder. Follow-up care should exclude the development of Crohn's disease or sarcoidosis.

Uterine fibroids can be treated with the same methods like sporadic uterine fibroids including antihormonal treatment, surgery or embolisation. Substantially elevated risk of progression to or independent development of uterine leiomyosarcoma has been reported which may influence treatment methods.

The predisposition to renal cell cancer calls for screening and, if necessary, urological management.

The skin lesions may be difficult to treat as they tend to recur after excision or destructive treatment. Drugs which affect smooth muscle contraction, such as doxazosin, nitroglycerine, nifedipine and phenoxybenzamine, may provide pain relief.

Topical lidocaine patches have been reported to decrease in severity and frequency of pain cutaneous leiomyomas.

A study by McKhann et al. compared the neurocognitive outcome of people with coronary artery disease (CAD) to heart-healthy controls (people with no cardiac risk factors). People with CAD were subdivided into treatment with CABG, OPCAB and non-surgical medical management. The three groups with CAD all performed significantly lower at baseline than the heart-healthy controls. All groups improved by 3 months, and there were minimal intrasubject changes from 3 to 12 months. No consistent difference between the CABG and off-pump patients was observed. The authors concluded patients with long-standing coronary artery disease have some degree of cognitive dysfunction secondary to cerebrovascular disease before surgery; there is no evidence the cognitive test performance of bypass surgery patients differed from similar control groups with coronary artery disease over a 12-month follow-up period. A related study by Selnes et al. concluded patients with coronary artery bypass grafting did not differ from a comparable nonsurgical control group with coronary artery disease 1 or 3 years after baseline examination. This finding suggests that late cognitive decline after coronary artery bypass grafting previously reported by Newman et al. may not be specific to the use of cardiopulmonary bypass, but may also occur in patients with very similar risk factors for cardiovascular and cerebrovascular disease.

Infantile Progressive Bulbar palsy is a rare type of progressive bulbar palsy that occurs in children. The disease exists in both rapid and slow onsets, and involves inflammation of the gray matter of the bulb. Infantile PBP is a disease that manifests itself in two forms: Fazio Londe syndrome (FL) and Brown-Vialetto-Van-Laere syndrome (BVVL).

Hennekam syndrome also known as intestinal lymphagiectasia–lymphedema–mental retardation syndrome, is an autosomal recessive disorder consisting of intestinal lymphangiectasia, facial anomalies, peripheral lymphedema, and mild to moderate levels of growth and intellectual disability.

It is also known as "lymphedema-lymphangiectasia-mental retardation syndrome".

In a subset of patients it is associated with CCBE1 according research published by its namesake, Raoul Hennekam. Other causal mutations were found in the FAT4 gene. Previously, mutations in the FAT4 gene had been only associated with van Maldergem syndrome. The molecular mechanism of the lymphedema phenotype in CCBE1-associated cases was identified as a diminished ability of the mutated CCBE1 to accelerate and focus the activation of the primary lymphangiogenic growth factor VEGF-C.

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.