Riluzole has been found to modestly prolong survival by approximately two to three months. It may have a greater survival benefit for those with a bulbar onset. It is approved by the US Food and Drug Administration (FDA) and recommended by the National Institute for Health and Care Excellence (NICE) (England and Wales). Riluzole does not reverse damage already done to motor neurons but affects neurons by reducing their activity through blocking Na+ entrance into the neurons and thus blocking the release of the chemicals that causes the activity of the motor neurons. The reduction in activity prevents the ruining of the neuronal muscle and so the drug can act as a protective chemical. Studies have shown that the function of this drug is dependent on the amount taken at a given time. The higher the concentration, the better the drug will protect the neurons from ruin. The recommended dosage of Riluzole is 50 mg, twice a day for people with known ALS for more than 5 years.

There are a number of side effects caused by the drug including the feeling of weakness in muscles but this is normal due to the function of the drug. Studies have shown that people on the drug are not likely to stop responding to it or develop symptoms that might cause the activity of neurons to rise again, making Riluzole an effective drug for prolonging survival.

In 2015, edaravone was approved in Japan for treatment of ALS after studying how and whether it works on 137 people with ALS and has obtained orphan drug status in the EU and USA. On May 5, 2017, the FDA approved edaravone to extend the survival period of people with ALS. It costs about 145,000 USD per year in the US and 35,000 USD per year in Japan.

Other medications may be used to help reduce fatigue, ease muscle cramps, control spasticity, and reduce excess saliva and phlegm. Drugs also are available to help people with pain, such as non-steroidal and anti-inflammatory drugs and opioids, depression, sleep disturbances, dysphagia, and constipation. Baclofen and diazepam are often prescribed to control the spasticity caused by ALS, and trihexyphenidyl, amitriptyline or most commonly glycopyrrolate may be prescribed when people with ALS begin having trouble swallowing their saliva. There is no evidence that medications are effective at reducing muscle cramps experienced by people with ALS.

Management of ALS attempts to relieve symptoms and extend life expectancy. This supportive care is best provided by multidisciplinary teams of healthcare professionals working with the person and their caregivers to keep them as mobile and comfortable as possible.

As of 2010, there was no cure for MMND. People with MMND are given supportive care to help them cope, which can include physical therapy, occupational therapy, counselling, and hearing aids.

Treatment of ALS2-related disorders includes physical therapy and occupational therapy to promote mobility and independence and use of computer technologies and devices to facilitate writing and voice communication.

Treatment for individuals with PLS is symptomatic. Baclofen and tizanidine may reduce spasticity. Quinine or phenytoin may decrease cramps. Some patients who do not receive adequate relief from oral treatment may consider intrathecal baclofen (i.e., infusion of medication directly into the cerebrospinal fluid via a surgically placed continuous infusion pump). However, patients are carefully selected for this type of procedure to ensure that they will likely benefit from this invasive procedure.

Physical therapy often helps prevent joint immobility. Speech therapy may be useful for those with involvement of the facial muscles. Physiotherapy treatment focuses on reducing muscle tone, maintaining or improving range of motion, increasing strength and coordination, and improving functional mobility. In PLS, stretching is thought to improve flexibility and can also reduce muscle spasticity and cramps.

Patients with PLS may find it beneficial to have an evaluation, as well as follow-up visits at multidisciplinary clinics, similar to those available for people with ALS. These multidisciplinary clinics may provide patients with the necessary treatment that they require by having an occupational therapist, physical therapist, speech language pathologist, dietician and nutritionist, all in one site.

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.

There is no known cure to BVVL however a Dutch group have reported the first promising attempt at treatment of the disorder with high doses of riboflavin. This Riboflavin protocol seems to be beneficial in almost all cases. Specialist medical advice is of course essential to ensure the protocol is understood and followed correctly.

Patients will almost certainly require additional symptomatic treatment and supportive care. This must be specifically customized to the needs of the individual but could include mobility aids, hearing aids or cochlear implants, vision aids, gastrostomy feeding and assisted ventilation, while steroids may or may not help patients.

The first report of BVVL syndrome in Japanese literature was of a woman that had BVVL and showed improvement after such treatments. The patient was a sixty-year-old woman who had symptoms such as sensorineural deafness, weakness, and atrophy since she was 15 years old. Around the age of 49 the patient was officially diagnosed with BVVL, incubated, and then attached to a respirator to improve her CO2 narcosis. After the treatments, the patient still required respiratory assistance during sleep; however, the patient no longer needed assistance by a respirator during the daytime.

Treatment is palliative, not curative (as of 2009).

Treatment options for lower limb weakness such as foot drop can be through the use of Ankle Foot Orthoses (AFOs) which can be designed or selected by an Orthotist based upon clinical need of the individual. Sometimes tuning of rigid AFOs can enhance knee stability.

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.

There is no known cure to DSMA1, and care is primarily supportive. Patients require respiratory support which may include non-invasive ventilation or tracheal intubation. The child may also undergo additional immunisations and offered antibiotics to prevent respiratory infections. Maintaining a healthy weight is also important. Patients are at risk of undernutrition and weight loss because of the increased energy spent for breathing. Physical and occupational therapy for the child can be very effective in maintaining muscle strength.

There is no published practice standard for the care in DSMA1, even though the Spinal Muscular Atrophy Standard of Care Committee has been trying to come to a consensus on the care standards for DSMA1 patients. The discrepancies in the practitioners’ knowledge, family resources, and differences in patient’s culture and/or residency have played a part in the outcome of the patient.

PBP is aggressive and relentless, and there were no treatments for the disease as of 2005. However, early detection of PBP is the optimal scenario in which doctors can map out a plan for management of the disease. This typically involves symptomatic treatments that are frequently used in many lower motor disorders.

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.

Since pseudobulbar palsy is a syndrome associated with other diseases, treating the underlying disease may eventually reduce the symptoms of pseudobulbar palsy.

Possible pharmacological interventions for pseudobulbar affect include the tricyclic antidepressants, serotonin reuptake inhibitors, and a novel approach utilizing dextromethorphan and quinidine sulfate. Nuedexta is an FDA approved medication for pseudobulbar affect. Dextromethorphan, an N-methyl-D-aspartate receptor antagonist, inhibits glutamatergic transmission in the regions of the brainstem and cerebellum, which are hypothesized to be involved in pseudobulbar symptoms, and acts as a sigma ligand, binding to the sigma-1 receptors that mediate the emotional motor expression.

The process of neurodegeneration is not well understood, so the diseases that stem from it have, as yet, no cures. In the search for effective treatments (as opposed to palliative care), investigators employ animal models of disease to test potential therapeutic agents. Model organisms provide an inexpensive and relatively quick means to perform two main functions: target identification and target validation. Together, these help show the value of any specific therapeutic strategies and drugs when attempting to ameliorate disease severity. An example is the drug Dimebon (Medivation). This drug is in phase III clinical trials for use in Alzheimer's disease, and also recently finished phase II clinical trials for use in Huntington's disease. In March 2010, the results of a clinical trial phase III were released; the investigational Alzheimer's disease drug Dimebon failed in the pivotal CONNECTION trial of patients with mild-to-moderate disease. With CONCERT, the remaining Pfizer and Medivation Phase III trial for Dimebon (latrepirdine) in Alzheimer's disease failed in 2012, effectively ending the development in this indication.

In another experiment using a rat model of Alzheimer's disease, it was demonstrated that systemic administration of hypothalamic proline-rich peptide (PRP)-1 offers neuroprotective effects and can prevent neurodegeneration in hippocampus amyloid-beta 25–35. This suggests that there could be therapeutic value to PRP-1.

Protein degradation offers therapeutic options both in preventing the synthesis and degradation of irregular proteins. There is also interest in upregulating autophagy to help clear protein aggregates implicated in neurodegeneration. Both of these options involve very complex pathways that we are only beginning to understand.

The goal of immunotherapy is to enhance aspects of the immune system. Both active and passive vaccinations have been proposed for Alzheimer's disease and other conditions, however more research must be done to prove safety and efficacy in humans.

One treatment methodogy that is very promising for the treatment of camptocormia is deep brain stimulation. Previously, deep brain stimulation and bilateral stimulation of the subthalamic nucleus and/or globus pallidus internus have been used to treat patients with Parkinson's disease. Studies have shown that similar treatments could be used on patients with severe camptocormia. By using the Burke-Fahn-Marsden Dystonia Rating Scale before and after treatment, it was found that patients experienced significant functional improvement in the ability to walk.

In the US, neuroborreliosis is typically treated with intravenous antibiotics which cross the blood–brain barrier, such as penicillins, ceftriaxone, or cefotaxime. One relatively small randomized controlled trial suggested ceftriaxone was more effective than penicillin in the treatment of neuroborreliosis. Small observational studies suggest ceftriaxone is also effective in children. The recommended duration of treatment is 14 to 28 days.

Several studies from Europe have suggested oral doxycycline is equally as effective as intravenous ceftriaxone in treating neuroborreliosis. Doxycycline has not been widely studied as a treatment in the US, but antibiotic sensitivities of prevailing European and US isolates of "Borrelia burgdorferi" tend to be identical. However, doxycycline is generally not prescribed to children due to the risk of bone and tooth damage.

Discreditied or doubtful treatments for neuroborreliosis include:

- Malariotherapy

- Hyperbaric oxygen therapy

- Colloidal silver

- Injections of hydrogen peroxide and bismacine

Because lack of sialic acid appears to be part of the pathology of IBM caused by GNE mutations, clinical trials with sialic acid supplements, and with a precursor of sialic acid, N-Acetylmannosamine, have been conducted, and as of 2016 further trials were planned.

Due to the wide range of causes of camptocormia, there is no one treatment that suits all patients. In addition, there is no specific pharmacological treatment for primary BSS. The use of analgesic drugs depends entirely on the intensity of the back pain. Muscular-origin BSS can be alleviated by positive lifestyle changes, including physical activity, walking with a cane, a nutritious diet, and weight loss. Worsening of symptoms is possible but rare in occurrence.

Treatment of the underlying cause of the disease can alleviate the condition in some individuals with secondary BSS. Other treatment options include drugs, injections of botulinum toxin, electroconvulsive therapy, deep brain stimulation, and surgical correction. Unfortunately, many of the elderly individuals affected by the BSS are not treated surgically due to age-related physical ailments and the long postoperative recovery period.

People with MMND become progressively more weak with time. Generally, affected individuals survive up to 30 years after they are diagnosed.

The importance of correctly recognizing progressive muscular atrophy as opposed to ALS is important for several reasons.

- 1) the prognosis is a little better. A recent study found the 5-year survival rate in PMA to be 33% (vs 20% in ALS) and the 10-year survival rate to be 12% (vs 6% in ALS).

- 2) Patients with PMA do not suffer from the cognitive change identified in certain groups of patients with MND.

- 3) Because PMA patients do not have UMN signs, they usually do not meet the "World Federation of Neurology El Escorial Research Criteria" for “Definite” or “Probable” ALS and so are ineligible to participate in the majority of clinical research trials such as drugs trials or brain scans.

- 4) Because of its rarity (even compared to ALS) and confusion about the condition, some insurance policies or local healthcare policies may not recognize PMA as being the life-changing illness that it is. In cases where being classified as being PMA rather than ALS is likely to restrict access to services, it may be preferable to be diagnosed as "slowly progressive ALS" or "lower motor neuron predominant" ALS.

An initial diagnosis of PMA could turn out to be slowly progressive ALS many years later, sometimes even decades after the initial diagnosis. The occurrence of upper motor neurone symptoms such as brisk reflexes, spasticity, or a Babinski sign would indicate a progression to ALS; the correct diagnosis is also occasionally made on autopsy.

There is no known cure for neuromyotonia, but the condition is treatable. Anticonvulsants, including phenytoin and carbamazepine, usually provide significant relief from the stiffness, muscle spasms, and pain associated with neuromyotonia. Plasma exchange and IVIg treatment may provide short-term relief for patients with some forms of the acquired disorder. It is speculated that the plasma exchange causes an interference with the function of the voltage-dependent potassium channels, one of the underlying issues of hyper-excitability in autoimmune neuromyotonia. Botox injections also provide short-term relief. Immunosuppressants such as Prednisone may provide long term relief for patients with some forms of the acquired disorder.

Research has focused on finding a pharmacological treatment that is specific for intention tremor. Limited success has been seen in treating intention tremor with drugs effective at treating essential tremor. Clinical trials of levetiracetam, typically used to treat epilepsy, and pramipexole, used to treat resting tremor, were completed in 2009-2010 to establish their effectiveness in treating kinetic tremor. A clinical trial for riluzole, typically used to treat amyotrophic lateral sclerosis, was completed at the Sapienza University of Rome to evaluate its effectiveness of treating cerebellar ataxia and kinetic tremor.

It is very difficult to treat an intention tremor. The tremor may disappear for a while after a treatment has been administered and then return. This situation is addressed with a different treatment. First, individuals will be asked if they use any of the drugs known to cause tremors. If so, they are asked to stop taking the medication and then evaluated after some time to determine if the medication was related to the onset of the tremor. If the tremor persists, treatment that follows may include drug therapy, lifestyle changes, and more invasive forms of treatment, such as surgery and thalamic deep brain stimulation.

Intention tremors are known to be very difficult to treat with pharmacotherapy and drugs. Although there is no established pharmacological treatment for an intention tremor, several drugs have been found to have positive effects on intention tremors and are used as treatment by many health professionals. Isoniazid, buspirone hydrochloride, glutethimide, carbamazepine, clonazepam, topiramate, zofran, propranolol and primidone have all seen moderate results in treating intention tremor and can be prescribed treatments. Isoniazid inhibits γ-aminobutyric acid-aminotransferase, which the first step in enzymatic breakdown of GABA, thus increasing GABA, the major inhibitory neurotransmitter in the central nervous system. This causes a reduction in cerebellar ataxias. Another neurotransmitter targeted by drugs that has been found to alleviate intention tremors is serotonin. The agonist buspirone hydrochloride, which decreases serotonin's function in the central nervous system, has been viewed as an effective treatment of intention tremors.

Physical therapy has had great results in reducing tremors but usually does not cure them. Relaxation techniques, such as meditation, yoga, hypnosis, and biofeedback, have seen some results with tremors. Wearing wrist weights which weigh down one's hands as they make movements, masking much of the tremor, is a proven home remedy. This is not a treatment, since wearing the weights does not have any lasting effects when they are not on. However, they do help the individual cope with the tremor immediately.

A more radical treatment that is used in individuals who do not respond to drug therapy, physical therapy, or any other treatment listed above, with moderate to severe intention tremors, is surgical intervention. Deep brain stimulation and surgical lesioning of the thalamic nuclei has been found to be an effective long-term treatment with intention tremors.

Deep brain stimulation treats intention tremors but does not help related diseases or disorders such as dyssynergia and dysmetria. Deep brain stimulation involves the implantation of a device called a neurostimulator, sometimes called a 'brain pacemaker'. It sends electrical impulses to specific parts of the brain, changing brain activity in a controlled manner. In the case of an intention tremor, the thalamic nuclei is the region targeted for treatment. This form of treatment causes reversible changes and does not cause any permanent lesions. Since it is reversible, deep brain stimulation is considered fairly safe: Reduction in tremor amplitude is almost guaranteed and sometimes resolved. Some individuals with multiple sclerosis have seen sustained benefits in MS progress.

Thalamotomy is another surgical treatment where lesions of the thalamus nucleus are created to disrupt the tremor circuit. Thalamotomy has been used to treat many forms of tremors, including those that arise from trauma, multiple sclerosis, stroke, and those whose cause it unknown. This is a very invasive, high-risk treatment with many negative effects, such as multiple sclerosis worsening, cognitive dysfunction, worsening of dysarthria, and dysphagia. Immediate positive effects are seen in individuals treated with a thalamotomy procedure. However, the tremor often comes back; it is not a complete treatment. Thalamotomy is in clinical trials to determine the validity of the treatment of intention tremors with all its high risks.

The treatment for post-polio syndrome is generally palliative and consists of rest, analgesia (pain relief) and utilisation of mechanisms to make life easier such as powered wheelchairs. There are no reversive therapies. Fatigue is usually the most disabling symptom; energy conservation can significantly reduce fatigue episodes. Such conservation can be achieved with lifestyle changes, reducing workload and daytime sleeping. Weight loss is also recommended if patients are obese. In some cases, the use of lower limb orthotics can reduce energy usage.

Medications for fatigue, such as amantadine and pyridostigmine, have not been found to be effective in the management of PPS. Muscle strength and endurance training are more important in managing the symptoms of PPS than the ability to perform long aerobic activity. Management should focus on treatments such as hydrotherapy and developing other routines that encourage strength but do not affect fatigue levels. The recent trend is towards use of intravenous immunoglobulin (IVIG) which has yielded promising, albeit modest results, but there is insufficient evidence to recommend it as a treatment.

PPS increases the stress on the musculoskeletal system due to increasing muscular atrophy. A recent study showed that in a review of 539 PPS patients, 80 percent reported pain in muscles and joints and 87 percent had fatigue. Joint instability can cause significant pain in individuals with PPS and should be adequately treated with painkillers. Supervised activity programs and decreasing mechanical stress with braces and adaptive equipment are recommended.

Because PPS can fatigue facial muscles, as well as cause dysphagia (difficulty swallowing), dysarthria (difficulty speaking) or aphonia (inability to produce speech), persons with PPS may become malnourished due to difficulty eating. Compensatory routines can help relieve these symptoms such as eating smaller portions at a time and sitting down whilst eating. PPS with respiratory involvement requires special management such as breathing exercises, chest percussion with a stethoscope on regular occasions for observation of the disease and management of secretions. Failure to properly assess PPS with respiratory involvement can increase the risk of missing aspiration pneumonia (an infection of the lower respiratory tract) in an individual. Severe cases may require permanent ventilation or tracheostomy. Sleep apnoea may also occur. Other management strategies that may lead to improvement include smoking cessation, treatment of other respiratory diseases and vaccination against respiratory infections such as influenza.

Patients can often live with PLS for many years and very often outlive their neurological disease and succumb to some unrelated condition. There is currently no effective cure, and the progression of symptoms varies. Some people may retain the ability to walk without assistance, but others eventually require wheelchairs, canes, or other assistive devices.