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.

Neurosarcoidosis, once confirmed, is generally treated with glucocorticoids such as prednisolone. If this is effective, the dose may gradually be reduced (although many patients need to remain on steroids long-term, frequently leading to side-effects such as diabetes or osteoporosis). Methotrexate, hydroxychloroquine, cyclophosphamide, pentoxifylline, thalidomide and infliximab have been reported to be effective in small studies. In patients unresponsive to medical treatment, radiotherapy may be required. If the granulomatous tissue causes obstruction or mass effect, neurosurgical intervention is sometimes necessary. Seizures can be prevented with anticonvulsants, and psychiatric phenomena may be treated with medication usually employed in these situations.

Cyclophosphamide is a drug often used in the treatment of lymphomas and works by slowing or stopping cell growth. It also works as an immunosuppressant by decreasing the body’s immune response to various diseases and conditions. This drug has been found to make significant improvements in people with anti-MAG neuropathy by relieving sensory loss and helping to improve quality of life in a few short months. There is, however, a risk of cancer because of this treatment and is therefore not used on a regular basis.

Fludarabine is a drug normally used to treat hematological malignancies and acts as an immunosuppressant. It has been shown to significantly improve conditions in neuropathy patients, but because of the lack of studies it is not used regularly. There is also a danger of potential toxicity as the treatment takes a year to stabilize the patient.

Management of neuropsychiatric lupus is similar to the management of neuropsychiatric disease in patients without lupus. Treatment depends on the underlying causes of a patient’s disease, and may include immunosuppressants, anticoagulants, and symptomatic therapy.

There is a wide range of treatments for central nervous system diseases. These can range from surgery to neural rehabilitation or prescribed medications.

Treatment typically involves improving the patient's quality of life. This is accomplished through the management of symptoms or slowing the rate of demyelination. Treatment can include medication, lifestyle changes (i.e. quit smoking, adjusting daily schedules to include rest periods and dietary changes), counselling, relaxation, physical exercise, patient education and, in some cases, deep brain thalamic stimulation (in the case of tremors). The progressive phase of MS appears driven by the innate immune system, which will directly contribute to the neurodegenerative changes that occur in progressive MS. Until now, there are no therapies that specifically target innate immune cells in MS. As the role of innate immunity in MS becomes better defined, it may be possible to better treat MS by targeting the innate immune system.

Treatments are patient-specific and depend on the symptoms that present with the disorder, as well as the progression of the condition.

Surgical excision of fatty tissue deposits around joints (liposuction) has been used in some cases. It may temporarily relieve symptoms although recurrences often develop.

Traditional analgesics

The pain in Dercum's disease is often reported to be refractory to analgesics and to non-steroidal anti-inflammatory drugs (NSAIDs). However, this has been contradicted by the findings of Herbst et al. They reported that the pain diminished in 89% of patients (n=89) when treated with NSAIDs and in 97% of patients when treated with narcotic analgesics (n=37). The dosage required and the duration of the pain relief are not precisely stated in the article.

Lidocaine

An early report from 1934 showed that intralesional injections of procaine (Novocain®) relieved pain in six cases. More recently, other types of local treatment of painful sites with lidocaine patches (5%) (Lidoderm®) or lidocaine/prilocaine (25 mg/25 mg) cream (EMLA®) have shown a reduction of pain in a few cases.

In the 1980s, treatment with intravenous infusions of lidocaine (Xylocaine®) in varying doses was reported in nine patients. The resulting pain relief lasted from 10 hours to 12 months. In five of the cases, the lidocaine treatment was combined with mexiletine (Mexitil®), which is a class 1B anti-arrhythmic with similar pharmacological properties as lidocaine.

The mechanism by which lidocaine reduces pain in Dercum's disease is unclear. It may block impulse conduction in peripheral nerves, and thereby disconnect abnormal nervous impulse circuits. Nonetheless, it might also depress cerebral activity that could lead to increased pain thresholds. Iwane et al. performed an EEG during the administration of intravenous lidocaine. The EEG showed slow waves appearing 7 minutes after the start of the infusion and disappearing within 20 minutes after the end of the infusion. On the other hand, the pain relief effect was the greatest at about 20 minutes after the end of the infusion.

Based on this, the authors concluded that the effect of lidocaine on peripheral nerves most likely explains why the drug has an effect on pain in Dercum's disease. In contrast, Atkinson et al. have suggested that an effect on the central nervous system is more likely, as lidocaine can depress consciousness and decrease cerebral metabolism. In addition, Skagen et al. demonstrated that a patient with Dercum's disease lacked the vasoconstrictor response to arm and leg lowering, which indicated that the sympathicusmediated local veno-arteriolar reflex was absent. This could suggest increased sympathetic activity. An infusion of lidocaine increased blood flow in subcutaneous tissue and normalised the vasoconstrictor response when the limbs were lowered. The authors suggested that the pain relief was caused by a normalisation of up-regulated sympathetic activity.

Methotrexate and infliximab

One patient's symptoms were improved with methotrexate and infliximab. However, in another patient with Dercum's disease, the effect of methotrexate was discreet. The mechanism of action is unclear. Previously, methotrexate has been shown to reduce neuropathic pain caused by peripheral nerve injury in a study on rats. The mechanism in the rat study case was thought to be a decrease in microglial activation subsequent to nerve injury. Furthermore, a study has shown that infliximab reduces neuropathic pain in patients with central nervous system sarcoidosis. The mechanism is thought to be mediated by tumour necrosis factor inhibition.

Interferon α-2b

Two patients were successfully treated with interferon α-2b. The authors speculated on whether the mechanism could be the antiviral effect of the drug, the production of endogenous substances, such as endorphins, or interference with the production of interleukin-1 and tumour necrosis factor. Interleukin-1 and tumour necrosis factor are involved in cutaneous hyperalgesia.

Corticosteroids

A few patients noted some improvement when treated with systemic corticosteroids (prednisolone), whereas others experienced worsening of the pain. Weinberg et al. treated two patients with juxta-articular Dercum's disease with intralesional injections of methylprednisolone (Depo-Medrol). The patients experienced a dramatic improvement.

The mechanism for the pain-reducing ability of corticosteroids in some conditions is unknown. One theory is that they inhibit the effects of substances, such as histamine, serotonin, bradykinin, and prostaglandins. As the aetiology of Dercum's disease is probably not inflammatory, it is plausible that the improvement some of the patients experience when using corticosteroids is not caused by an anti-inflammatory effect.

Most patients reported in the literature have been given treatments suitable for autoimmune neurological diseases, such as corticosteroids, plasmapheresis and/or intravenous immunoglobulin, and most have made a good recovery. The condition is too rare for controlled trials to have been undertaken.

A range of medications that act on the central nervous system has been found to be useful in managing neuropathic pain. Commonly used treatments include tricyclic antidepressants (such as nortriptyline or amitriptyline), the serotonin-norepinephrine reuptake inhibitor (SNRI) medication duloxetine, and antiepileptic therapies such as gabapentin, pregabalin, or sodium valproate. Few studies have examined whether nonsteroidal anti-inflammatory drugs are effective in treating peripheral neuropathy.

Symptomatic relief for the pain of peripheral neuropathy may be obtained by application of topical capsaicin. Capsaicin is the factor that causes heat in chili peppers. The evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option. Local anesthesia often is used to counteract the initial discomfort of the capsaicin. Some current research in animal models has shown that depleting neurotrophin-3 may oppose the demyelination present in some peripheral neuropathies by increasing myelin formation.

High-quality evidence supports the use of cannabis for neuropathic pain.

Since each case is different, the following are possible treatments that patients might receive in the management of myelitis.

- Intravenous steroids

High-dose intravenous methyl-prednisolone for 3–5 days is considered as a standard of care for patients suspected to have acute myelitis, unless there are compelling reasons otherwise. The decision to offer continued steroids or add a new treatment is often based on the clinical course and MRI appearance at the end of 5 days of steroids.

- Plasma exchange (PLEX)

Patients with moderate to aggressive forms of disease who don’t show much improvement after being treated with intravenous and oral steroids will be treated with PLEX. Retrospective studies of patients with TM treated with IV steroids followed by PLEX showed a positive outcome. It also has been shown to be effective with other autoimmune or inflammatory central nervous system disorders. Particular benefit has been shown with patients who are in the acute or subacute stage of the myelitis showing active inflammation on MRI. However, because of the risks implied by the lumbar puncture procedure, this intervention is determined by the treating physician on a case-by-case basis.

- Immunosuppressants/Immunomodulatory agents

Myelitis with no definite cause seldom recurs, but for others, myelitis may be a manifestation of other diseases that are mentioned above. In these cases, ongoing treatment with medications that modulate or suppress the immune system may be necessary. Sometimes there is no specific treatment. Either way, aggressive rehabilitation and long-term symptom management are an integral part of the healthcare plan.

In terms of treatment for neuromuscular diseases (NMD), "exercise" might be a way of managing them, as NMD individuals would gain muscle strength. In a study aimed at results of exercise, in muscular dystrophy and Charcot-Marie-Tooth disease, the later benefited while the former did not show benefit; therefore, it depends on the disease Other management routes for NMD should be based on medicinal and surgical procedures, again depending on the underlying cause.

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.

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.

Treatment also involves central nervous system penetrating chemotherapy. Options include intrathecal, intraventricular, and systemic chemotherapy. These must penetrate the blood-brain barrier in order to be effective. Sometimes mixing multiple forms of treatment with chemotherapy seems to be the best route. For example, some significant improvement has been shown as a result of cranial radiation treatment preceding a brief course of intrathecal chemotherapy. Although this is an effective treatment to do, penetrating the blood-brain barrier can cause side effects due to the toxicity in the nervous system. These would include dizziness, confusion, and changes in mental status. Another form could be the use of pharmaceuticals, which have all shown positive results for treatment but should always be consulted with a physician to asses risks.

Exercise is a promising mechanism of prevention and treatment for various diseases characterized by neuroinflammation. Aerobic exercise is used widely to reduce inflammation in the periphery. Exercise has been shown to decreases proliferation of microglia in the brain, decrease hippocampal expression of immune-related genes, and reduce expression of inflammatory cytokines such as TNF-α.

Autologous stem-cell transplants are shown to be an effective treatment. However, this should be only considered for certain people due to toxicity concerns. It is possible that the transplant may cause problems like septic shock.

It is expected that there will be no new cases of progressive inflammatory neuropathy since the process of aerosolizing the pig brains has been discontinued at all pork processing facilities.

Proper treatment of autonomic dysreflexia involves administration of anti-hypertensives along with immediate determination and removal of the triggering stimuli. Often, sitting the patient up and dangling legs over the bedside can reduce blood pressures below dangerous levels and provide partial symptom relief. Tight clothing and stockings should be removed. Straight catheterization of the bladder every 4 to 6 hrs, or relief of a blocked urinary catheter tube may resolve the problem. The rectum should be cleared of stool impaction, using anaesthetic lubricating jelly. If the noxious precipitating trigger cannot be identified, drug treatment is needed to decrease elevating intracranial pressure until further studies can identify the cause.

Drug treatment includes the rapidly acting vasodilators, including sublingual nitrates or oral clonidine. Ganglionic blockers are also used to control sympathetic nervous system outflow. Topical nitropaste is a convenient and safe treatment—an inch or two can be applied to the chest wall, and wiped off when blood pressures begin to normalize. Autonomic dysreflexia is abolished temporarily by spinal or general anaesthesia. These treatments are used during obstetric delivery of a woman with autonomic dysreflexia.

Should the viral progression be diagnosed during stage 1 (even during late stage 1 when stage 2 symptoms start to manifest themselves) then treatment to combat the infection can be administered successfully—there is no cure for SSPE but if it is caught early enough then the sufferer can respond to the treatment and prevent symptom recurrence by taking the medication for the rest of their life. The treatment for the SSPE infection is the immunomodulator interferon and specific antiviral medication—ribavirin and inosine pranobex are specifically used to greater effect than antivirals such as amantadine.

For those who have progressed to stage 2 or beyond, the disease is incurable. For patients in the terminal phase of the disease there is a palliative care and treatment scheme—this involves anticonvulsant therapy (to help with the body's progressive loss of control of the nervous system causing gradually more intensive spasms/convulsions) alongside supportive measures to help maintain vital functioning. It is fairly standard as the infection spreads and symptoms intensify that feeding tubes need to be inserted to keep a nutritional balance. As the disease progresses to its most advanced phase, the patient will need constant nursing as normal bodily function declines to the complete collapse of the nervous system.

Combinations of treatment for SSPE include:

- Oral inosine pranobex (oral isoprinosine) combined with intrathecal (injection through a lumbar puncture into the spinal fluid) or intraventricular interferon alpha.

- Oral inosine pranobex (oral isoprinosine) combined with interferon beta.

- Intrathecal interferon alpha combined with intravenous ribavirin.

In October 2007 an astute medical interpreter noticed similar neurological symptoms being reported by Spanish-speaking patients seeking treatment from different physicians at the Austin Medical Center, in Austin, Minnesota. Not only did these patients share similar neurological symptoms, they also worked at the same pork processing plant. Dr. Daniel LaChance, a physician at both the Austin Medical Center and the Mayo Clinic in nearby Rochester, Minnesota, was notified. He launched a request to area physicians to refer other patients with similar symptoms to him. The Minnesota Department of Health (MDH) was notified and began an investigation into the "outbreak." The MDH identified workers from two other pork processing plants in Indiana and Nebraska who also had parallel neurological complaints. Several agencies including the Occupational Safety and Health Administration (OSHA) and the Center for Disease Control and Prevention (CDC) were brought in to assist. Simultaneously investigations were conducted to rule out contagious disease, to locate the source or carrier, and to identify what exactly was causing these workers to develop these symptoms.

Removal from exposure was the first line of treatment. Due to progressive sensory loss and weakness, immunotherapy was often required. These treatments included intravenous methylprednisolone, oral prednisone, azathioprine, and/or immunoglobulin. All 24 patients improved, including 7 who received no treatment and 17 who required immunotherapy.

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.

Gene-based therapies for patients with HSAN I are not available to date, hence supportive care is the only treatment available for the patients. Ulcero-mutilating complications are the most serious, prominent, and leading diagnostic features in HSAN I. Since the complications mimic foot ulcers caused by diabetic neuropathy, the treatment for foot ulcers and infections can follow the guidelines given for diabetic foot care which starts with early and accurate counseling of patients about risk factors for developing foot ulcerations. Orthopedic care and the use of well fitting shoes without pressure points should also be included. Recently, the treatment of the foot complications has reached an efficient level allowing treatment on an outpatient basis. Early treatment of the foot complications often avoids hospitalization and, in particular, amputations. In sum, the principles of the treatment are removal of pressure to the ulcers, eradication of infection, and specific protective footwear afterwards.

Of the phenomena occurring in neurosarcoid, only facial nerve involvement is known to have a good prognosis and good response to treatment. Long-term treatment is usually necessary for all other phenomena. The mortality rate is estimated at 10%