Typical tumefactive lesions have been found to be responsive to corticosteroids because of their immunosuppressive and anti-inflammatory properties. They restore the blood-brain barrier and induce cell death of T-cells.

No standard treatment exists, but practitioners seem to apply intravenous corticosteroids, followed by plasmapheresis and cyclophosphamide in non-responsive cases High dose intravenous corticosteroids (methylprednisolone 1 g for 3–5 days) followed by oral tapering hasten clinical and radiological improvement in approximately 80% of patients

Plasmapheresis has been reported to work even in the absence of response to corticosteroids

The treatment of spasticity ranges from physical activity to medication. Physical activity includes stretching, aerobic exercises and relaxation techniques. Currently, there is little understanding as to why these physical activities aid in relieving spasticity. Medical treatments include baclofen, diazepam and dantrolene which is a muscle-relaxant. Dantrolene has many side effects and as such, it is usually not the first choice in treatment of spasticity. The side effects include dizziness, nausea and weakness.

Electrical stimulation can promote nerve regeneration. The frequency of stimulation is an important factor in the success of both quality and quantity of axon regeneration as well as growth of the surrounding myelin and blood vessels that support the axon. Histological analysis and measurement of regeneration showed that low frequency stimulation had a more successful outcome than high frequency stimulation on regeneration of damaged sciatic nerves.

Surgery can be done in case a nerve has become cut or otherwise divided. Recovery of a nerve after surgical repair depends mainly on the age of the patient. Young children can recover close-to-normal nerve function. In contrast, a patient over 60 years old with a cut nerve in the hand would expect to recover only protective sensation, that is, the ability to distinguish hot/cold or sharp/dull. Many other factors also affect nerve recovery. The use of autologous nerve grafting procedures that involve redirection of regenerative donor nerve fibers into the graft conduit has been successful in restoring target muscle function. Localized delivery of soluble neurotrophic factors may help promote the rate of axon regeneration observed within these graft conduits.

An expanding area of nerve regeneration research deals with the development of scaffolding and bio-conduits. Scaffolding developed from biomaterial would be useful in nerve regeneration if they successfully exhibit essentially the same role as the endoneurial tubes and Schwann cell do in guiding regrowing axons.

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)

In terms of the management of spinal and bulbar muscular atrophy, no cure is known and treatment is supportive. Rehabilitation to slow muscle weakness can prove positive, though the prognosis indicates some individuals will require the use of a wheelchair in later stages of life.

Surgery may achieve correction of the spine, and early surgical intervention should be done in cases where prolonged survival is expected. Preferred nonsurgical treatment occurs due to the high rate of repeated dislocation of the hip.

Practical surgical procedures used for treating synkinesis are neurolysis and selective myectomy. Neurolysis has been shown to be effective in relieving synkinesis but only temporarily and unfortunately symptoms return much worse than originally. Selective myectomy, in which a synkinetic muscle is selectively resected, is a much more effective technique that can provide permanent relief and results in a low recurrence rate; unfortunately, it also has many post-operative complications that can accompany including edema, hematoma, and ecchymosis. Therefore, surgical procedures are very minimally used by doctors and are used only as last-resort options for patients who do not respond well to non-invasive treatments.

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

Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy.

Physical therapists can assist patients in maintaining their level of independence through therapeutic exercise programmes. One recent research report demonstrated a gain of 2 SARA points (Scale for the Assessment and Rating of Ataxia) from physical therapy. In general, physical therapy emphasises postural balance and gait training for ataxia patients. General conditioning such as range-of-motion exercises and muscle strengthening would also be included in therapeutic exercise programmes. Research showed that spinocerebellar ataxia 2 (SCA2) patients with a mild stage of the disease gained significant improvement in static balance and neurological indices after six months of a physical therapy exercise training program. Occupational therapists may assist patients with incoordination or ataxia issues through the use of adaptive devices. Such devices may include a cane, crutches, walker, or wheelchair for those with impaired gait. Other devices are available to assist with writing, feeding, and self care if hand and arm coordination are impaired. A randomised clinical trial revealed that an intensive rehabilitation program with physical and occupational therapies for patients with degenerative cerebellar diseases can significantly improve functional gains in ataxia, gait, and activities of daily living. Some level of improvement was shown to be maintained 24 weeks post-treatment. Speech language pathologists may use both behavioral intervention strategies as well as augmentative and alternative communication devices to help patients with impaired speech.

Botox (botulinum toxin) is a new and versatile tool for the treatment of synkinesis. Initially used for reducing hyperkinesis after facial palsy, Botox was later attempted on patients with post-facial palsy synkinesis to reduce unwanted movements. The effects of Botox have shown to be remarkable, with synkinetic symptoms disappearing within 2 or 3 days. The most common treatment targets are the orbicularis oculi, depressor anguli oris (DAO), mentalis, platysma and the contralateral depressor labii inferioris muscles. Due to the short span of Botox effects though, patients must come back to the doctor for re-injection approximately every 3 months. More notable is that in a majority of patients, various synkinetic movements completely disappeared after 2-3 sessions of trimonthly Botox injections.

A more specific synkinesis, crocodile tears syndrome (hyperlacrimation upon eating), has been shown to respond exceedingly well to Botox injection. Botox is injected directly into the lacrimal gland and has shown to reduce hyperlacrimation within 24–48 hours. The procedure was shown to be simple and safe with very little chance of side-effects (although on rare occasions ptosis can occur due to botulinum toxin diffusion). Furthermore, reduction in hyper-lacrimation was shown to last longer than the expected 3 months (about 12 months).

Since Botox can mimic facial paralysis, an optimized dose has been determined that reduces involuntary synkinesis of the muscle while not affecting muscle tone.

There is no cure for spinocerebellar ataxia, which is currently considered to be a progressive and irreversible disease, although not all types cause equally severe disability.

In general, treatments are directed towards alleviating symptoms, not the disease itself. Many patients with hereditary or idiopathic forms of ataxia have other symptoms in addition to ataxia. Medications or other therapies might be appropriate for some of these symptoms, which could include tremor, stiffness, depression, spasticity, and sleep disorders, among others. Both onset of initial symptoms and duration of disease are variable. If the disease is caused by a polyglutamine trinucleotide repeat CAG expansion, a longer expansion may lead to an earlier onset and a more radical progression of clinical symptoms. Typically, a person afflicted with this disease will eventually be unable to perform daily tasks (ADLs). However, rehabilitation therapists can help patients to maximize their ability of self-care and delay deterioration to certain extent. Researchers are exploring multiple avenues for a cure including RNAi and the use of Stem Cells and several other avenues.

On January 18, 2017 BioBlast Pharma announced completion of Phase 2a clinical trials of their medication, Trehalose, in the treatment of SCA3. BioBlast has received FDA Fast Track status and Orphan Drug status for their treatment. The information provided by BioBlast in their research indicates that they hope this treatment may prove efficacious in other SCA treatments that have similar pathology related to PolyA and PolyQ diseases.

In addition, Dr. Beverly Davidson has been working on a methodology using RNAi technology to find a potential cure for over 2 decades. Her research began in the mid-1990s and progressed to work with mouse models about a decade later and most recently has moved to a study with non-human primates. The results from her most recent research "are supportive of clinical application of this gene therapy". Dr. Davidson along with Dr. Pedro Gonzalez-Alegre are currently working to move this technique into a Phase 1 clinical trial.

Finally, another gene transfer technology discovered in 2011 has also been shown by Dr. Davidson to hold great promise and offers yet another avenue to a potential future cure.

Neurapraxia is often treated and cured by non-operative means. The primary goals of treatment are to maintain the proper nutrition of the paralyzed muscles, prevent contraction by the antagonists of the paralyzed muscles, and to consistently keep the joints mobile. A splint is often used in cases of neurapraxia because it is able to maintain a relaxed position of the paralyzed muscle. The splint prevents the paralyzed muscle from being overstretched either by the force of gravity or by other non-paralyzed antagonists. During the recovery period of neurapraxia, it is essential that the joints constantly undergo passive movement in order to preserve proper mobility. If joints are kept mobile, the limb has the best possible chance of benefit from the return of nervous function. Non-steroidal anti-inflammatory medications can also help to reduce swelling at the injury site. In addition to these non-operative remedies, it is suggested that muscles affected by neurapraxia be kept warm at all times. Circulation in the limb is stimulated with the use of heat.

Once voluntary movement has returned to the muscle, recovery and treatment continues by the participation in active exercises. Physical Therapy and Occupational Therapy are common sources of treatment during these early stages of restoration of active movement. Almost all cases of neurapraxia can be completely treated by non-operative means.

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People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

Because the exact cause of CBD is unknown, there exists no formal treatment for the disease. Instead, treatments focus on minimizing the appearance or effect of the symptoms resulting from CBD. The most easily treatable symptom of CBD is parkinsonism, and the most common form of treatment for this symptom is the application of dopaminergic drugs. However, in general only moderate improvement is seen and the relief from the symptom is not long-lasting. In addition, palliative therapies, including the implementation of wheelchairs, speech therapy, and feeding techniques, are often used to alleviate many of the symptoms that show no improvement with drug administration.

A 2006 study followed 223 patients for a number of years. Of these, 15 died, with a median age of 65 years. The authors tentatively concluded that this is in line with a previously reported estimate of a shortened life expectancy of 10-15 years (12 in their data).

Transneuronal degeneration is the death of neurons resulting from the disruption of input from or output to other nearby neurons. It is an active excitotoxic process when a neuron is overstimulated by a neurotransmitter (most commonly glutamate) causing the dysfunction of that neuron (either damaging it or killing it) which drives neighboring neurons into metabolic deficit, resulting in rapid, widespread loss of neurons. This can be either anterograde or retrograde, indicating the direction of the degeneration relative to the original site of damage (see types). There are varying causes for transneuronal degeneration such as brain lesions, disconnection syndromes, respiratory chain deficient neuron interaction, and lobectomies. Although there are different causes, transneuronal degeneration generally results in the same effects (whether they be cellular, dendritic, or axonal) to varying degrees. Transneuronal degeneration is thought to be linked to a number of diseases, most notably Huntington's disease and Alzheimer's disease, and researchers recently have been performing experiments with monkeys and rats, monitoring lesions in different parts of the body to study more closely how exactly the process works.

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.

Wallerian degeneration is a process that results when a nerve fiber is cut or crushed and the part of the axon distal to the injury (i.e. farther from the neuron's cell body) degenerates. This is also known as anterograde or orthograde degeneration. A related process known as 'Wallerian-like degeneration' occurs in many neurodegenerative diseases, especially those where axonal transport is impaired. Primary culture studies suggest that a failure to deliver sufficient quantities of the essential axonal protein NMNAT2 is a key initiating event.

Wallerian degeneration occurs after axonal injury in both the peripheral nervous system (PNS) and central nervous system (CNS). It occurs in the axon stump distal to a site of injury and usually begins within 24–36 hours of a lesion. Prior to degeneration, distal axon stumps tend to remain electrically excitable. After injury, the axonal skeleton disintegrates, and the axonal membrane breaks apart. The axonal degeneration is followed by degradation of the myelin sheath and infiltration by macrophages. The macrophages, accompanied by Schwann cells, serve to clear the debris from the degeneration.

Schwann cells respond to loss of axons by extrusion of their myelin sheaths, downregulation of myelin genes, dedifferentiation and proliferation. They finally align in tubes (Büngner bands) and express surface molecules that guide regenerating fibers. Within 4 days of the injury, the distal end of the portion of the nerve fiber proximal to the lesion sends out sprouts towards those tubes and these sprouts are attracted by growth factors produced by Schwann cells in the tubes. If a sprout reaches the tube, it grows into it and advances about 1 mm per day, eventually reaching and reinnervating the target tissue. If the sprouts cannot reach the tube, for instance because the gap is too wide or scar tissue has formed, surgery can help to guide the sprouts into the tubes. Regeneration is efficient in the PNS, with near complete recovery in case of lesions that occur close to the distal nerve terminal. However recovery is hardly observed at all in the spinal cord. One crucial difference is that in the CNS, including the spinal cord, myelin sheaths are produced by oligodendrocytes and not by Schwann cells.

According to medical professionals with the Cleveland Clinic, once an athlete suffers from an episode of cervical spinal cord, team physician or athletic trainer first stabilize the head and neck followed by a thorough neurologic inspection. If the injury is deemed severe, injured parties should be taken to a hospital for evaluation. Athletes that suffer from severe episodes of neurapraxia are urged to consult orthopaedic or spinal medical specialists. In mild cases of neurapraxia, the athlete is able to remove themselves from the field of play. However, the athlete is still advised to seek medical consultation.

Corneal transplant surgery may be difficult due to the peripheral thinning of the cornea, even with large and off-center grafts. Therefore, surgery is usually reserved for patients that do not tolerate contact lenses. Several different surgical approaches may be taken, and no one approach is currently established as the standard. Examples of surgical procedures used for PMD include: wedge resection, lamellar crescentic resection, penetrating keratoplasty, lamellar keratoplasty, epikeratoplasty and intracorneal segments. Transplantation of the entire thickness of the cornea (penetrating keratoplasty) may be performed if there is enough normal tissue present. However, if there is not enough normal tissue present, then attaching the graft is difficult.

Due to the thinning of the cornea, PMD patients are poor candidates for procedures such as LASIK and photorefractive keratectomy.

Orthotics and corticosteroid injections are widely used conservative treatments for Morton’s neuroma. In addition to traditional orthotic arch supports, a small foam or fabric pad may be positioned under the space between the two affected metatarsals, immediately behind the bone ends. This pad helps to splay the metatarsal bones and create more space for the nerve so as to relieve pressure and irritation. It may however also elicit mild uncomfortable sensations of its own, such as the feeling of having an awkward object under one's foot. Corticosteroid injections can relieve inflammation in some patients and help to end the symptoms. For some patients, however, the inflammation and pain recur after some weeks or months, and corticosteroids can only be used a limited number of times because they cause progressive degeneration of ligamentous and tendinous tissues.

Sclerosing alcohol injections are an increasingly available treatment alternative if the above management approaches fail. Dilute alcohol (4%) is injected directly into the area of the neuroma, causing toxicity to the fibrous nerve tissue. Frequently, treatment must be performed 2–4 times, with 1–3 weeks between interventions. A 60–80% success rate has been achieved in clinical studies, equal to or exceeding the success rate for surgical neurectomy with fewer risks and less significant recovery. If done with more concentrated alcohol under ultrasound guidance, the success rate is considerably higher and fewer repeat procedures are needed.

Radio Frequency Ablation is also used in the treatment of Morton's Neuroma The outcomes appear to be equally or more reliable than alcohol injections especially if the procedure is done under ultrasound guidance.

If such interventions fail, patients are commonly offered surgery known as neurectomy, which involves removing the affected piece of nerve tissue. Postoperative scar tissue formation (known as stump neuroma) can occur in approximately 20%-30% of cases, causing a return of neuroma symptoms. Neurectomy can be performed using one of two general methods. Making the incision from the dorsal side (the top of the foot) is the more common method but requires cutting the deep transverse metatarsal ligament that connects the 3rd and 4th metatarsals in order to access the nerve beneath it. This results in exaggerated postoperative splaying of the 3rd and 4th digits (toes) due to the loss of the supporting ligamentous structure. This has aesthetic concerns for some patients and possible though unquantified long-term implications for foot structure and health. Alternatively, making the incision from the ventral side (the sole of the foot) allows more direct access to the affected nerve without cutting other structures. However, this approach requires a greater post-operative recovery time where the patient must avoid weight bearing on the affected foot because the ventral aspect of the foot is more highly enervated and impacted by pressure when standing. It also has an increased risk that scar tissue will form in a location that causes ongoing pain.

Cryogenic neuroablation is a lesser known alternative to neurectomy surgery. Cryogenic neuroablation (also known as cryo injection therapy, cryoneurolysis, cryosurgery or cryoablation) is a term that is used to describe the destruction of axons to prevent them from carrying painful impulses. This is accomplished by making a small incision (~3 mm) and inserting a cryoneedle that applies extremely low temperatures of between −50 °C to −70 °C to the nerve/neuroma. This results in degeneration of the intracellular elements, axons, and myelin sheath (which houses the neuroma) with wallerian degeneration. The epineurium and perineurium remain intact, thus preventing the formation of stump neuroma. The preservation of these structures differentiates cryogenic neuroablation from surgical excision and neurolytic agents such as alcohol. An initial study showed that cryo neuroablation is initially equal in effectiveness to surgery but does not have the risk of stump neuroma formation.

Recently, an increasing number of procedures are being performed at specialist centers which offer a range of procedures to treat Morton's neuroma under ultrasound guidance. Recent studies have shown excellent results for the treatment of Morton's neuroma with ultrasound guided sclerosing alcohol injections, ultrasound guided radiofrequency ablation, and ultrasound guided cryo-ablation.

The severe pain of HNA can be controlled with an anti-inflammatory drug such as prednisone, although it is unknown whether these anti-inflammatory drugs actually slow or stop the nerve degeneration process.

Nerve regeneration after an episode is normal, and in less severe cases a full recovery of the nerves and muscles can be expected. However, in a severe case permanent nerve damage may occur.

There is evidence suggesting corneal collagen cross-linking may be beneficial for patients with pellucid marginal degeneration. Research shows some promising results by combining collagen cross linking with photorefractive keratectomy, or with topography-guided transepithelial surface ablation.

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

Laser treatment of drusen has been studied. While it is possible to eliminate drusen with this treatment strategy, it has been shown that this fails to reduce the risk of developing the choroidal neovascularisation which causes the blindness associated with age-related macular degeneration.