There is currently no known pharmacological treatment to hereditary motor and sensory neuropathies. However, the majority of people with these diseases are able to walk and be self-sufficient. Some methods of relief for the disease include physical therapy, stretching, braces, and sometimes orthopedic surgery. Since foot disorders are common with neuropathy disorders precautions must be taken to strengthen these muscles and use preventative care and physical therapy to prevent injury and deformities.

Hereditary motor and sensory neuropathies are relatively common and are often inherited with other neuromuscular conditions, and these co morbidities cause an accelerated progression of the disease.

Most forms HMSN affects males earlier and more severely than females, but others show no predilection to either sex. HMSN affects all ethnic groups. With the most common forms having no racial prediliections, but other recessively inherited forms tend to impact specific ethnic groups. Onset of HMSN in most common in early childhood, with clinical effects occurring before the age of 10, but some symptoms are lifelong and progress slowly. Therefore, these symptoms do not appear until later in life.

Deep brain stimulation (DBS) is a technique that uses electrodes placed in the brain to modify brain activity by sending a constant electrical signal to the nearby nuclei. Treatment of muscle tone issues via deep brain stimulation typically targets the global pallidus and has shown to significantly improve symptoms associated with ADCP. The specific mechanism by which DBS affects ADCP is unclear. DBS of the globus pallidus interna improves dystonia in people with dyskinetic CP in 40% of cases, perhaps due to variation in basal ganglia injuries.

Medications that impede the release of excitatory neurotransmitters have been used to control or prevent spasms. Treatment with intrathecal baclofen, a gamma-aminobutyric acid (GABA) agonist, decreases muscle tone and has been shown to decrease the frequency of muscle spasms in ADCP patients. Tetrabenazine, a drug commonly used in the treatment of Huntington's disease, has been shown to be effective treating chorea.

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.

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.

Current forms of prevention are focused during pregnancy, while others are focused immediately after birth. Some methods that have been used include prolonging the pregnancy using interventions such as 17-alpha progesterone, limiting the number of gestations during pregnancy (for pregnancies induced by assistive reproductive technology), antenatal steroid for mothers likely to deliver prematurely, high caffeine for premature births with extremely low birth weights.

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.

Although no cure exists, there are many different treatments which are currently being used to help control symptoms. These include short term treatment with some drugs (such as Botox) which relax the muscles, use of temperature changes to control muscle tremors, and a balanced approach of coordinated care and support involving physical therapists, orthopedic surgeons, and psychiatrists.

Because there is no cure for ataxic cerebral palsy, current methods of treatment are diverse, often consisting of multiple focuses designed to limit the severity of symptoms. Many children suffering from ataxic cerebral palsy are treated by teams consisting of individuals from numerous disciplines, including physical therapists, occupational therapist, orthopedic surgeons, and psychiatrists. Treatment by such teams involves multiple approaches. Providing a primary care medical home to support children suffering from common symptoms of nutritional deficiencies, pain, dental care, bowel and bladder continence, and orthopedic complications is an essential aspect of treatment. In addition, utilizing diagnostic techniques to identify the nature and severity of brain abnormalities has become increasingly beneficial for treatment in recent years.

Different medications have been used to temporarily treat ataxic cerebral palsy. Medications like primidone and benzodiazepine, while not recommended for long term use, can alleviate some of the tremor symptoms. Botox which relaxes tightened muscles has been effective in treating voice, hand and head tremors. A few recently published papers outlined a potential method for treating intention tremor which consisted of cooling the forearm by wrapping it in a cryomanchet using a circulating fluid. After the treatment most patients experienced reduced tremor for up to half an hour. This practical, however short-term treatment can facilitate performing normal daily activities like applying make up, eating, or signing documents. This potential treatment method is also significant in that it reduces one’s reliance on caregivers.

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.

In some cases Meige's syndrome can be reversed when it is caused by medication. It has been theorized that it is related to cranio-mandibular orthopedic misalignment, a condition that has been shown to cause a number of other movement disorders (Parkinon's, tourettes, and torticollis). This theory is supported by the fact that the trigeminal nerve is sensory for blink reflex, and becomes hypertonic with craniomandibular dysfunction. Palliative treatments are available, such as botulinum toxin injections.

Left untreated, tabes dorsalis can lead to paralysis, dementia, and blindness. Existing nerve damage cannot be reversed.

Schwann cells provide the nerve with protection through the production of Nerve Growth Factors, and because these cells are intact this kind of nerve injury can be cured and normal feeling and sensations can be restored. Surgery can be done in order to help the nerve heal. The surgery will help with nerve regeneration, providing guidance to the nerve sprouts on where to attach on the proximal side of the injury. Damaged nerve axons can reattach themselves after surgery. Treatment of axonotmesis also consists of:

- Physical therapy or Occupational Therapy. Physical or Occupational therapy aims include:

- Pain relief

- Maintain range of motion

- Reducing muscular atrophy

- Patient education

- Use of assistive devices (Orthotic needs)

The prognosis is usually good in terms of recovery. Rate of recovery depends on the distance from the site of injury, and axonal regeneration can go up to 1 inch per month. Complete recovery can take anywhere from 6 months to a year

It can reduce the effectiveness of the sodium-channel blocker lidocaine in dental work, so the amide-type local anesthetic. articaine is used on victims instead.

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.

Intravenously administered penicillin is the treatment of choice. Associated pain can be treated with opiates, valproate, or carbamazepine. Those with tabes dorsalis may also require physical therapy to deal with muscle wasting and weakness. Preventive treatment for those who come into sexual contact with an individual with syphilis is important.

In terms of prognosis radial neuropathy is not necessarily permanent, though sometimes there could be partial loss of movement/sensation.Complications may be possible deformity of the hand in some individuals.

If the injury is axonal (the underlying nerve fiber itself is damaged) then full recovery may take months or years ( or could be permanent). EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery.

The use of oral potassium and avoiding high carbohydrate meals can help treat it according to resent tests. Dr. Jacob O. Levitt, a dermatologist who has hypokalemic periodic paralysis, recently conducted research in to it.

Treatment of TSP involves corticosteroids to help with inflammation. Though any success with corticosteroids is short-lived, with symptoms worsened as the dosage is reduced. A synthetic derivative, 17-alpha-ethinyltestosterone, can be used to treat Tropical spastic paraparesis, improvement in motor and bladder function was reported but not sustainable.

Mogamulizumab, an anti-CCR4 IgG1 monoclonal antibody, is also being researched as a possible treatment for Tropical spastic paraparesis. The antibody reduces HTLV-1 proviral load and production of proinflammatory cytokines. Valproic acid has also succeeded in reducing the proviral load of HTLV-1 (though clinical benefits were minimal or none). A further combination of valproic acid and zidovudine has demonstrated a decrease in proviral loads (in animals).

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.

At the time of the report there was no known treatment for the disease; specifically, it was not established whether steroids were helpful or harmful. Other techniques such as plasmaphoresis, intravenous immunoglobulin, and experimental antiviral drugs have been attempted on a trial basis, but have not been reported to be effective. On November 7 the CDC issued "Interim Considerations for Clinical Management of Patients with Acute Flaccid Myelitis", based on "consensus guidance drawn from experts in infectious diseases, neurology, pediatrics, critical care medicine, public health epidemiology and virology." Mark Sawyer of the American Academy of Pediatrics, who contributed to the guidance, was quoted by the organization's newsletter: The most important issue summarized in the document is that there is no clear evidence that therapies intended to modify the immune system (e.g., corticosteroids, immune globulin, plasmapheresis) have a beneficial effect in this condition. Plasmapheresis is specifically not recommended because the potential for harm is significant in the absence of any evidence of benefit.