Treatment usually consists of observation unless the patient has concern, there is pain, drainage, or other symptoms related to the lesion. Surgical removal of the affected gland would be recommended in those cases. Another treatment option would be aspiration, which can be repeated multiple times. This is commonly performed in those who are debilitated or in those whose benefit from surgery would be outweighed by the risks. Prognosis is usually good; rarely this condition may devolve into lymphoma, or could actually represent 'occult' lymphoma from the outset.

Corticosteroids remain the main treatment modality for IOI. There is usually a dramatic response to this treatment and is often viewed as pathognomonic for this disease. Although response is usually quick, many agree that corticosteroids should be continued on a tapering basis to avoid breakthrough inflammation.

Although many respond to corticosteroid treatment alone, there are several cases in which adjuvant therapy is needed. While many alternatives are available, there is no particular well-established protocol to guide adjuvant therapy. Among the available options there is: surgery, alternative corticosteroid delivery, radiation therapy, non-steroidal anti-inflammatory drugs, cytotoxic agents (chlorambucil, cyclophosphamide), corticosteroid sparing immunosuppressants (methotrexate, cyclosporine, azathioprine), IV immune-globin, plasmapheresis, and biologic treatments (such as TNF-α inhibitors).

The treatment of dysautonomia can be difficult; since it is made up of many different symptoms, a combination of drug therapies is often required to manage individual symptomatic complaints. Therefore, if an autoimmune neuropathy is the case, then treatment with immunomodulatory therapies is done, or if diabetes mellitus is the cause, control of blood glucose is important. Treatment can include proton-pump inhibitors and H2 receptor antagonists used for digestive symptoms such as acid reflux.

For the treatment of genitourinary autonomic neuropathy medications may include sildenafil (a guanine monophosphate type-5 phosphodiesterase inhibitor). For the treatment of hyperhidrosis, anticholinergic agents such as trihexyphenidyl or scopolamine can be used, also intracutaneous injection of botulinum toxin type A can be used for management in some cases.

Balloon angioplasty, a procedure referred to as transvascular autonomic modulation, is specifically not approved for the treatment of autonomic dysfunction.

If the cause of dacryoadenitis is a viral condition such as mumps, simple rest and warm compresses may be all that is needed. For other causes, the treatment is specific to the causative disease.

A DCR is the treatment of choice for most patients with acquired NLD obstruction. Surgical indications include recurrent dacryocystitis, chronic mucoid reflux, painful distension of the lacrimal sac, and bothersome epiphora. For patients with dacryocystitis, active infection should be cleared, if possible, before DCR is performed.

While there is no cure for JBS, treatment and management of specific symptoms and features of the disorder are applied and can often be successful. Variability in the severity of JBS on a case-by-case basis determines the requirements and effectiveness of any treatment selected.

Pancreatic insufficiency and malabsorption can be managed with pancreatic enzyme replacement therapy, such as pancrelipase supplementation and other related methods.

Craniofacial and skeletal deformities may require surgical correction, using techniques including bone grafts and osteotomy procedures. Sensorineural hearing loss can be managed with the use of hearing aids and educational services designated for the hearing impaired.

Special education, specialized counseling methods and occupational therapy designed for those with mental retardation have proven to be effective, for both the patient and their families. This, too, is carefully considered for JBS patients.

Mumps can be prevented by immunization. Gonococcus, bacteria can be avoided by the use of condoms. Most other causes cannot be prevented.

Some clinicians believe that partial stenosis of the NLD with symptomatic epiphora sometimes responds to surgical intubation of the entire lacrimal drainage system. This procedure should be performed only if the tubes can be passed easily. In complete NLD obstruction, intubation alone is not effective, and a DCR should be considered.

The adrenal glands atrophy during prolonged use of exogenous glucocorticoids like prednisone. Atrophy of the breasts can occur with prolonged estrogen reduction, as with anorexia nervosa or menopause. Testicular atrophy with prolonged use of enough exogenous sex steroid (either androgen or estrogen) to reduce gonadotropin secretion.

One drug in test seemed to prevent the type of muscle loss that occurs in immobile, bedridden patients.

Testing on mice showed that it blocked the activity of a protein present in the muscle that is involved in muscle atrophy. However, the drug's long-term effect on the heart precludes its routine use in humans, and other drugs are being sought.

Since December 2016, autosomal recessive proximal spinal muscular atrophy can be treated with nusinersen. No cure is known to any of the remaining disorders of the spinal muscular atrophies group. The main objective there is to improve quality of life which can be measured using specific questionnaires. Supportive therapies are widely employed for patients who often also require comprehensive medical care involving multiple disciplines, including pulmonology, neurology, orthopedic surgery, critical care, and clinical nutrition. Various forms of physiotherapy and occupational therapy are frequently able to slow down the pace of nerve degeneration and muscle wasting. Patients also benefit greatly from the use of assistive technology.

Pharmacological methods of treatment include fludrocortisone, midodrine, somatostatin, erythropoietin, and other vasopressor agents. However, often a patient with pure autonomic failure can mitigate his or her symptoms with far less costly means. Compressing the legs and lower body, through crossing the legs, squatting, or the use of compression stockings can help. Also, ingesting more water than usual can increase blood pressure and relieve some symptoms.

Muscle atrophy can be opposed by the signaling pathways which induce muscle hypertrophy, or an increase in muscle size. Therefore, one way in which not exercise induces an increase in muscle mass is to down regulate the pathways which have the opposite effect.

β-hydroxy β-methylbutyrate (HMB), a metabolite of leucine which is sold as a dietary supplement, has demonstrated efficacy in preventing the loss of muscle mass in several muscle wasting conditions in humans, particularly sarcopenia. A growing body of evidence supports the efficacy of HMB as a treatment for reducing, or even reversing, the loss of muscle mass, muscle function, and muscle strength in hypercatabolic disease states such as cancer cachexia; consequently, it is recommended that both the prevention and treatment of sarcopenia and muscle wasting in general include supplementation with HMB, regular resistance exercise, and consumption of a high-protein diet. Based upon a meta-analysis of seven randomized controlled trials that was published in 2015, HMB supplementation has efficacy as a treatment for preserving lean muscle mass in older adults. More research is needed to determine the precise effects of HMB on muscle strength and function in this age group.

Since the absence of muscle-building amino acids can contribute to muscle wasting (that which is torn down must be rebuilt with like material), amino acid therapy may be helpful for regenerating damaged or atrophied muscle tissue. The branched-chain amino acids or BCAAs (leucine, isoleucine, and valine) are critical to this process, in addition to lysine and other amino acids.

In severe cases of muscular atrophy, the use of an anabolic steroid such as methandrostenolone may be administered to patients as a potential treatment. A novel class of drugs, called SARM (selective androgen receptor modulators) are being investigated with promising results. They would have fewer side-effects, while still promoting muscle and bone tissue growth and regeneration. These claims are, however, yet to be confirmed in larger clinical trials.

One important rehabilitation tool for muscle atrophy includes the use of functional electrical stimulation to stimulate the muscles. This has seen a large amount of success in the rehabilitation of paraplegic patients.

Currently there is no effective therapy for dominant optic atrophy, and consequently, these patients are simply monitored for changes in vision by their eye-care professional. Children of patients should be screened regularly for visual changes related to dominant optic atrophy. Research is underway to further characterize the disease so that therapies may be developed.

Although no specific treatment exists, the disease can be managed with anticonvulsants, physiotherapy, etc.

The successful treatment of xerostomia is difficult to achieve and often unsatisfactory. This involves finding any correctable cause and removing it if possible, but in many cases it is not possible to correct the xerostomia itself, and treatment is symptomatic, and also focuses on preventing tooth decay through improving oral hygiene. Where the symptom is caused by hyposalivation secondary to underlying chronic disease, xerostomia can be considered permanent or even progressive. The management of salivary gland dysfunction may involve the use of saliva substitutes and/or saliva stimulants:

- Saliva substitutes – these include SalivaMAX, water, artificial salivas (mucin-based, carboxymethylcellulose-based), and other substances (milk, vegetable oil).

- Saliva stimulants – organic acids (ascorbic acid, malic acid), chewing gum, parasympathomimetic drugs (choline esters, e.g. pilocarpine hydrochloride, cholinesterase inhibitors), and other substances (sugar-free mints, nicotinamide).

Saliva substitutes can improve xerostomia, but tend not to improve the other problems associated with salivary gland dysfunction. Parasympathomimitic drugs (saliva stimulants) such as pilocarpine may improve xerostomia symptoms and other problems associated with salivary gland dysfunction, but the evidence for treatment of radiation-induced xerostomia is limited. Both stimulants and substitutes relieve symptoms to some extent. Salivary stimulants are probably only useful in people with some remaining detectable salivary function. A systematic review of the treatment of dry mouth found no strong evidence to suggest that a specific topical therapy is effective. The review reported limited evidence that oxygenated glycerol triester spray was more effective than electrolyte sprays. Sugar free chewing gum increases saliva production but there is no strong evidence that it improves symptoms. There is a suggestion that intraoral devices and integrated mouthcare systems may be effective in reducing symptoms, but there was a lack of strong evidence. A systematic review of the management of radiotherapy induced xerostomia with parasympathomimetic drugs found that there was limited evidence to support the use of pilocarpine in the treatment of radiation-induced salivary gland dysfunction. It was suggested that, barring any contraindications, a trial of the drug be offered in the above group (at a dose of five mg three times per day to minimize side effects). Improvements can take up to twelve weeks. However, pilocarpine is not always successful in improving xerostomia symptoms. The review also concluded that there was little evidence to support the use of other parasympathomimetics in this group.

A 2013 review looking at non-pharmacological interventions reported a lack of evidence to support the effects of electrostimulation devices, or acupuncture, on symptoms of dry mouth.

Benign lymphoepithelial lesion is a type of benign enlargement of the parotid and/or lacrimal glands. This pathologic state is sometimes, but not always, associated with Sjögren's syndrome.

Brown atrophy of the heart is atrophy of the heart muscle (or myocardium) commonly found in the elderly. It is described as brown because fibers become pigmented by intracellular lipofuscin deposits (mostly around the cell nucleus) a type of lipochrome granule.

It has no known effect on function, and is described as being expected or normal in aging.

Other types of brown atrophy include brown atrophy of neuronia and brown atrophy of the liver.

Multifocal motor neuropathy is normally treated by receiving intravenous immunoglobulin (IVIG), which can in many cases be highly effective, or immunosuppressive therapy with cyclophosphamide or rituximab. Steroid treatment (prednisone) and plasmapheresis are no longer considered to be useful treatments; prednisone can exacerbate symptoms. IVIg is the primary treatment, with about 80% of patients responding, usually requiring regular infusions at intervals of 1 week to several months. Other treatments are considered in case of lack of response to IVIg, or sometimes because of the high cost of immunoglobulin. Subcutaneous immunoglobulin is under study as a less invasive, more-convenient alternative to IV delivery.

Though there is no treatment for Cone dystrophy, certain supplements may help in delaying the progression of the disease.

The beta-carotenoids, lutein and zeaxanthin, have been evidenced to reduce the risk of developing age related macular degeneration (AMD), and may therefore provide similar benefits to Cone dystrophy sufferers.

Consuming omega-3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid) has been correlated with a reduced progression of early AMD, and in conjunction with low glycemic index foods, with reduced progression of advanced AMD, and may therefore delay the progression of cone dystrophy.

Moisture replacement therapies such as artificial tears may ease the symptoms of dry eyes. Some patients with more severe problems use goggles to increase local humidity or have punctal plugs inserted to help retain tears on the ocular surface for a longer time.

Additionally, cyclosporine (Restasis) is available by prescription to help treat chronic dry eye by suppressing the inflammation that disrupts tear secretion. Prescription drugs are also available that help to stimulate salivary flow, such as cevimeline (Evoxac) and pilocarpine. Salagen, a manufactured form of pilocarpine, can be used to help produce tears, as well as saliva in the mouth and intestines. It is derived from the jaborandi plant.

In women with SS, vaginal dryness, vulvodynia and dyspareunia (painful sexual intercourse) are often reported; personal lubricants are recommended to help lessen irritation or pain that may result from dryness in the vaginal and vulva areas.

Salivary gland aplasia (also termed salivary gland agenesis) is the congenital absence of salivary glands. Usually the term relates to the absence of some or all of the major salivary glands.

It is a rare condition, and most known cases have been in association with syndromes of the ectodermal tissues, particularly the lacrimal apparatus. Example syndromes which have been reported with salivary gland aplasia include hereditary ectodermal dysplasia, mandibulofacial dysostosis and hemifacial microsomia.

The main significance of the condition is a lack of saliva, causing xerostomia (dry mouth), with accompanying susceptibility to dental caries (tooth decay), infections of the mouth, and upper respiratory tract infections (e.g., candidiasis, ascending sialadenitis, laryngitis and pharyngitis). Patients with salivary gland aplasia typically require regular application of topical fluoride to prevent tooth decay.

Treatment can occur in two ways: treating symptoms and treating the deficiency. Treatment of symptoms usually includes the use of artificial tears in the form of eye drops, increasing the humidity of the environment with humidifiers, and wearing wraparound glasses when outdoors. Treatment of the deficiency can be accomplished with a Vitamin A or multivitamin supplement or by eating foods rich in Vitamin A. Treatment with supplements and/or diet can be successful until the disease progresses as far as corneal ulceration, at which point only an extreme surgery can offer a chance of returning sight.

Like many mitochondrial diseases, there is no cure for MERRF, no matter the means for diagnosis of the disease. The treatment is primarily symptomatic. High doses of Coenzyme Q10, B complex vitamins and L-Carnitine are the drugs that patients are treated with in order to account for the altered metabolic processed resulting in the disease. There is very little success with these treatments as therapies in hopes of improving mitochondrial function. The treatment only alleviates symptoms and these do not prevent the disease from progressing. Patients with concomitant disease, such as diabetes, deafness or cardiac disease, are treated in combination to manage symptoms.