Plasmapheresis and intravenous immunoglobulins (IVIG) are the two main immunotherapy treatments for GBS. Plasmapheresis attempts to reduce the body's attack on the nervous system by filtering antibodies out of the bloodstream. Similarly, administration of IVIG neutralizes harmful antibodies and inflammation. These two treatments are equally effective, but a combination of the two is not significantly better than either alone. Plasmapheresis speeds recovery when used within four weeks of the onset of symptoms. IVIG works as well as plasmapheresis when started within two weeks of the onset of symptoms, and has fewer complications. IVIG is usually used first because of its ease of administration and safety. Its use is not without risk; occasionally it causes liver inflammation, or in rare cases, kidney failure. Glucocorticoids alone have not been found to be effective in speeding recovery and could potentially delay recovery.

While pain is common in people with Guillain–Barré syndrome, studies comparing different types of pain medication are insufficient to make a recommendation as to which should be used.

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.

AMAN, also known as Chinese Paralytic Syndrome, was first described by a group of Johns Hopkins University and University of Pennsylvania neurologists in collaboration with neurologists from the Second Teaching Hospital of Hebei Medical School and Beijing Children's Hospital. In 1991, Guy Mckhann, Jack Griffin, Dave Cornblath and Tony Ho from Johns Hopkins University and Arthur Asbury from University of Pennsylvania visited China to study a mysterious epidemic of paralytic syndrome occurring in northern China. Every summer, hundreds of children from rural China developed acute paralysis and respiratory failure. Hospitals were overwhelmed with number of cases and often ran out of ventilators and hospital beds. Examination of these children showed that many of them had acute flaccid paralysis and areflexia but with little or no sensory loss. Electrophysiological testing of these children showed motor axonal loss with occasional conduction block with a lack of demyelinating features and normal sensory potentials. In contrast, the common form of Guillain–Barré syndrome in the West often presents with sensory loss and demyelination on electrophysiology testing and is more common in adults. Later, several autopsies confirmed the focus of the immune attack was at the motor axolemma especially around the nodes of Ranvier. These cases showed deposition of antibody and complement along the motor axolemma and associated macrophage infiltration.

Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically, there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier.

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.

Transcutaneous electrical nerve stimulation therapy may be effective and safe in the treatment of diabetic peripheral neuropathy. A recent review of three trials involving 78 patients found some improvement in pain scores after 4 and 6, but not 12 weeks of treatment and an overall improvement in neuropathic symptoms at 12 weeks. Another review of four trials found significant improvement in pain and overall symptoms, with 38% of patients in one trial becoming asymptomatic. The treatment remains effective even after prolonged use, but symptoms return to baseline within a month of cessation of treatment.

In the treatment of polyneuropathies one must ascertain and manage the cause, among management activities are: weight decrease, use of a walking aid, and occupational therapist assistance. Additionally BP control in those with diabetes is helpful, while intravenous immunoglobulin is used for multifocal motor neuropathy.

According to Lopate, et al., methylprednisolone is a viable treatment for chronic inflammatory demyelinative polyneuropathy (which can also be treated with intravenous immunoglobulin) The author(s) also indicate that prednisone has greater adverse effects in such treatment, as opposed to intermittent (high-doses) of the aforementioned medication.

According to Wu, et al., in critical illness polyneuropathy supportive and preventive therapy are important for the affected individual, as well as, avoiding (or limiting) corticosteroids.

First-line treatment for CIDP is currently intravenous immunoglobulin (IVIG) and other treatments include corticosteroids (e.g. prednisone), and plasmapheresis (plasma exchange) which may be prescribed alone or in combination with an immunosuppressant drug. Recent controlled studies show subcutaneous immunoglobin (SCIG) appears to be as effective for CIDP treatment as IVIG in most patients, and with fewer systemic side effects.

IVIG and plasmapheresis have proven benefit in randomized, double-blind, placebo-controlled trials. Despite less definitive published evidence of efficacy, corticosteroids are considered standard therapies because of their long history of use and cost effectiveness. IVIG is probably the first-line CIDP treatment, but is extremely expensive. For example, in the U.S., a single 65 g dose of Gamunex brand in 2010 might be billed at the rate of $8,000 just for the immunoglobulin—not including other charges such as nurse administration. Gamunex brand IVIG is the only U.S. FDA approved treatment for CIDP, as in 2008 Talecris, the maker of Gamunex, received orphan drug status for this drug for the treatment of CIDP.

Immunosuppressive drugs are often of the cytotoxic (chemotherapy) class, including rituximab (Rituxan) which targets B cells, and cyclophosphamide, a drug which reduces the function of the immune system. Ciclosporin has also been used in CIDP but with less frequency as it is a newer approach. Ciclosporin is thought to bind to immunocompetent lymphocytes, especially T-lymphocytes.

Non-cytotoxic immunosuppressive treatments usually include the anti-rejection transplant drugs azathioprine (Imuran/Azoran) and mycophenolate mofetil (Cellcept). In the U.S., these drugs are used as "off-label" treatments for CIDP, meaning that their use here is accepted by the FDA, but that CIDP treatment is not explicitly indicated or approved in the drug literature. Before azathioprine is used, the patient should first have a blood test that ensures that azathioprine can safely be used.

Anti-thymocyte globulin (ATG), an immunosuppressive agent that selectively destroys T lymphocytes is being studied for use in CIDP. Anti-thymocyte globulin is the gamma globulin fraction of antiserum from animals that have been immunized against human thymocytes. It is a polyclonal antibody.

Although chemotherapeutic and immunosuppressive agents have shown to be effective in treating CIDP, significant evidence is lacking, mostly due to the heterogeneous nature of the disease in the patient population in addition to the lack of controlled trials.

A review of several treatments found that azathioprine, interferon alpha and methotrexate were not effective. Cyclophosphamide and rituximab seem to have some response. Mycophenolate mofetil may be of use in milder cases. Immunoglobulin and steroids are the first line choices for treatment. Rarely bone marrow transplantation has been performed.

Physical therapy and occupational therapy may improve muscle strength, activities of daily living, mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints.

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.

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.

Bickerstaff brainstem encephalitis is a rare inflammatory disorder of the central nervous system, first described by Edwin Bickerstaff in 1951. It may also affect the peripheral nervous system, and has features in common with both Miller Fisher syndrome and Guillain–Barré syndrome.

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.

In 1982 Lewis et al reported a group of patients with a chronic asymmetrical sensorimotor neuropathy mostly affecting the arms with multifocal involvement of peripheral nerves. Also in 1982 Dyck "et al" reported a response to prednisolone to a condition they referred to as chronic inflammatory demyelinating polyradiculoneuropathy. Parry and Clarke in 1988 described a neuropathy which was later found to be associated with IgM autoantibodies directed against GM1 gangliosides. This latter condition was later termed multifocal motor neuropathy This distinction is important because multifocal motor neuropathy responds to intravenous globulin alone while chronic inflammatory demyelinating polyneuropathy responds to intravenous globulin, steroids and plasma exchanges. It has been suggested that multifocal motor neuropathy is distinct from chronic inflammatory demyelinating polyneuropathy and that Lewis-Summer syndrome is a distinct variant type of chronic inflammatory demyelinating polyneuropathy.

The Lewis-Summer form of this condition is considered a rare disease with only 50 cases reported up to 2004. A total of 90 cases had been reported by 2009

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.

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.

Surgical decompression can give excellent results if the clinical picture and the EMG suggest a compression neuropathy.

In brachial plexus neuritis, conservative management may be more appropriate.

Spontaneous recovery has been reported, but is said to be delayed and incomplete.

There is a role for physiotherapy and this should be directed specifically towards the pattern of pain and symptoms. Soft tissue massage, stretches and exercises to directly mobilise the nerve tissue may be used.⁠

Polyneuropathy ( + + ) is damage or disease affecting peripheral nerves (peripheral neuropathy) in roughly the same areas on both sides of the body, featuring weakness, numbness, and burning pain. It usually begins in the hands and feet and may progress to the arms and legs; and sometimes to other parts of the body where it may affect the autonomic nervous system. It may be acute or chronic. A number of different disorders may cause polyneuropathy, including diabetes and some types of Guillain–Barré syndrome.

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.

Treatment for hemiparesis is the same treatment given to those recovering from strokes or brain injuries. Health care professionals such as physical therapists and occupational therapists play a large role in assisting these patients in their recovery. Treatment is focused on improving sensation and motor abilities, allowing the patient to better manage their activities of daily living. Some strategies used for treatment include promoting the use of the hemiparetic limb during functional tasks, maintaining range of motion, and using neuromuscular electrical stimulation to decrease spasticity and increase awareness of the limb. At the more advanced level, using constraint-induced movement therapy will encourage overall function and use of the affected limb. Mirror Therapy (MT) has also been used early in stroke rehabilitation and involves using the unaffected limb to stimulate motor function of the hemiparetic limb. Results from a study on patients with severe hemiparesis concluded that MT was successful in improving motor and sensory function of the distal hemiparetic upper limb. Active participation is critical to the motor learning and recovery process, therefore it’s important to keep these individuals motivated so they can make continual improvements.

Also speech pathologists work to increase function for people with hemiparesis.

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Physical therapy is the predominant treatment of symptoms. Orthopedic shoes and foot surgery can be used to manage foot problems.

An occurrence of Todd's paralysis indicates that a seizure has occurred. The prognosis for the patient depends upon the effects of the seizure, not the occurrence of the paralysis.

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.

Those diseases understood as congenital in origin could either be specific to the ocular organ system (LHON, DOA) or syndromic (MELAS, Multiple Sclerosis). It is estimated that these inherited optic neuropathies in the aggregate affect 1 in 10,000

Of the acquired category, disease falls into further etiological distinction as arising from toxic (drugs or chemicals) or nutritional/metabolic (vitamin deficiency/diabetes) insult. It is worth mentioning that under-nutrition and toxic insult can occur simultaneously, so a third category may be understood as having a combined or mixed etiology. We will refer to this as Toxic/Nutritional Optic Neuropathy, whereby nutritional deficiencies and toxic/metabolic insults are the simultaneous culprits of visual loss associated with damage and disruption of the RGC and optic nerve mitochondria.

There is currently no cure for FD and death occurs in 50% of the affected individuals by age 30. There are only two treatment centers, one at New York University Hospital and one at the Sheba Medical Center in Israel. One is being planned for the San Francisco area.

The survival rate and quality of life have increased since the mid-1980s mostly due to a greater understanding of the most dangerous symptoms. At present, FD patients can be expected to function independently if treatment is begun early and major disabilities avoided.

A major issue has been aspiration pneumonia, where food or regurgitated stomach content would be aspirated into the lungs causing infections. Fundoplications (by preventing regurgitation) and gastrostomy tubes (to provide nonoral nutrition) have reduced the frequency of hospitalization.

Other issues which can be treated include FD crises, scoliosis, and various eye conditions due to limited or no tears.

An FD crisis is the body's loss of control of various autonomic nervous system functions including blood pressure, heart rate, and body temperature. Both short-term and chronic periodic high or low blood pressure have consequences and medication is used to stabilize blood pressure.